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Meg Mangin R.N.
Research Team
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Posted: Sun Mar 20th, 2005 21:15 |
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My kidney function tests are worse since I started the MP. What should I do?
Immunopathology reveals kidney inflamation
Because most kidney inflammation/disease is 'silent', it is not uncommon for subclinical kidney inflammation to be exacerbated due to unavoidable immunopathology as part of the recovery process with the Marshall Protocol. The problem is noticed when lab work indicating kidney function comes back abnormal.
All infections and antibiotic courses for them can cause elevations in BUN and creatinine. When kidney function tests are worse, indicating increased inflammation, this is actually a good sign because it means the MP is working.
Reduced kidney function is caused by the disease, not directly by Benicar or the other antibacterial drugs. Angiotensin Receptor Blockers (ARBs) such as Benicar are used to slow kidney injury due to disease, because ARBs relax delicate blood vessels in the kidneys and rebalance Th1 homeostasis by blocking Angiotensin II, a hormone with a profibrotic effect.
"Patients with Th1 disease have a high risk of kidney inflammation. This inflammation is often occult (subclinical) and only becomes evident when inflammation increases with the immunopathology of recovery. Many Th1 patients are surprised when they find out how much their kidneys have been affected by the disease.
Most Doctors have no idea how sick their Th1 patients really are. They have no idea of the amount of kidney disease, as the tests for kidney function are unbelievably crude for this day and age.
The kidneys of Th1 patients are almost always weak, some of them extremely weak. But none have 'failed', because the weak kidneys are revealing themselves as part of the healing process, and they are protected by the ARB (Benicar), and the reactivated innate immune system.
Kidneys are one of the tissues which suffer significant fibrosis (collagen deposition)(scarring) during Th1 diseases. Most Th1 patients have significant kidney damage, even if there is no sign of it until the bacteria start to be killed. The kidney issues resolve as the disease resolves."
Dr. Trevor Marshall, Ph.D.
Kidney function tests
Creatinine
Creatinine has been found to be a fairly reliable indicator of kidney function although someone can have a “normal” creatinine and decreased kidney function.
As the kidneys become impaired, the creatinine level in the blood will rise. Abnormally high levels of creatinine thus warn of possible malfunction of the kidneys, often before a patient reports any symptoms.
*Normal levels of creatinine in the blood are approximately:
Adult males 0.6 to 1.2mg/dL (53-106umol/L)
Adult females 0.5 to 1.1mg/dL (44-97umol/L)
*Reference ranges will vary by laboratory.
Note: The units used in the United States are milligrams per deciliter (mg/dl). To convert to international units (micromoles perliter multiply the creatinine (in mg/dl) by 88. Thus a serum creatinine of 2mg/dl is the same as 176 micromoles per liter (umol/L).
Drugs that can falsely elevate creatinine include: cimetidine, trimethoprim-sulfa (Bactrim), and nephrotoxic drugs, such as cephalosporins (cefoxitin)
Estimated Glomerular Filtration Rate (eGFR)
The estimated glomerular filtration rate (eGFR) is a more accurate assessment of how efficiently the kidneys are filtering wastes from the blood and is the measurement used to evaluate kidney function.
The National Kidney Disease Education Program (NKDEP) of the National Institute of Diabetes and Diseases of the Kidney (NIDDK), National Kidney Foundation (NKF) and American Society of Nephrology (ASN) recommend estimating GFR from serum creatinine using the MDRD Study equation. This equation uses serum creatinine in combination with age, sex and race to estimate GFR.
The normal GFR in both kidneys in healthy adults is 120 to 125 mL/min. The lower the GFR number, the worse the kidney function.
A standard reference range is not available for this test. Because reference values are dependent on many factors, including patient age, gender, sample population, and test method, numeric test results have different meanings in different labs. Your lab report should include the specific reference range for your test.
The eGFR has limitations
Although the estimated GFR is often a more accurate estimate of kidney function than the serum creatinine alone, it has its limitations. The formula used to calculate it is very sensitive to the serum creatinine and can be dramatically affected by lab errors when the creatinine is relatively normal. Also, it assumes a certain body type based on the persons age, gender and race but this may not be true. For example, if you are a very tiny woman with very little muscles, you may be producing a lot less creatinine than the average woman with a similar age and racial background.
The MDRD equation can be considered reasonably accurate if certain conditions are met:
-Your Creatinine Is Stable: It is assumed that the amount of creatinine you are making is equal to the amount being removed by your kidneys. This is not true if you have an acute or sudden kidney failure or you are on dialysis.
-You are Similar to the Study Subjects: Since the MDRD equation was defined using a group real people, it is most accurate if you have similar characteristics. Examples include:
-You don't have an unusual diet (i.e. vegetarian diet, high protein, creatine supplements)
-You are not very thin or very overwieght
-You don't have paraplegia, amputations, or a muscle disease
-You don't have severe liver disease
-You are over 18 years of age
The lower the GFR number, the worse the kidney function but the equations are not as accurate when the results are greater than 60 mL/min/1.73m2.
National Kidney Foundation Definition of Chronic Kidney Disease
Kidney damage for three or more months, as defined by structural or functional abnormalities of the kidney, with or without decreased GFR, manifested by pathologic abnormalities or markers of kidney damage, including abnormalities in the composition of the blood or urine or abnormalities in imaging tests. GFR < 60 mL per minute per 1.73 m2 for three months or more, with or without kidney damage.
The stages of chronic kidney disease (CKD) are defined based on the level the eGFR and other factors.
See Guideline to eGFR levels while treating kidney inflammation
Creatinine Clearance
The 24 hour Creatinine Clearance test compares the level of creatinine in urine with the creatinine level in the blood, usually based on measurements of a 24-hour urine sample and a blood sample drawn at the end of the 24-hour period.
Creatinine clearance may be needed to estimate the GFR in the following conditions:
-Extremes of age and body size
-Severe malnutrition or obesity
-Disease of skeletal muscle
-Paraplegia or quadriplegia
-Vegetarian diet
-Rapidly changing kidney function
Blood Urea Nitrogen (BUN)
Urea is a by-product of protein metabolism. This waste product is formed in the liver, then filtered from the blood and excreted in the urine by the kidneys. The BUN test measures the amount of nitrogen contained in the urea. High BUN levels can indicate kidney dysfunction, but because blood urea nitrogen is also affected by protein intake and liver function, the test is usually done in conjunction with a blood creatinine, a more specific indicator of kidney function.
BUN is often high because nitric oxide is one of the components given off by dying bacteria and apoptosing white cells, as nitric oxide is one of the byproducts of the endotoxin inflammation.
BUN lab range: 7 to 20 milligrams per deciliter (mg/dL) or mmol/L
BUN/creatinine ratio
The ratio of BUN to creatinine needs to be evaluated in view of the clinical picture. The reference range is a variable 6:1 to 20:1
In normal kidney function, creatinine stays the same and BUN varies.
Osmolality and osmolarity
The osmolality urine test the concentration of particles in urine. Osmolality (particles/kg water) and osmolarity (particles/liter of solution) are sometimes confused, but for dilute fluids such as urine they are essentially the same.
Urine osmolality reflects the total number of osmotically active particles in the urine, without regard to the size or weight of the particles. Substances such as glucose, proteins, or dyes increase the urinary specific gravity. Therefore, urine osmolality is a more accurate measurement of urine concentration than specific gravity
It is normally maintained under precise control by homeostatic mechanisms involving stimulation of thirst, secretion of antidiuretic hormone (ADH), and renal handling of filtered sodium and potassium. Elevation may indicate syndrome of inappropriate antidiuretic hormone secretion (SIADH). Lower-than-normal measurements may indicate aldosteronism (very rare), diabetes insipidus (rare), excess fluid intake, renal tubular necrosis or severe pyelonephritis.
Normal values are as follows:
-Random specimen: 50 to 1400 milliosmoles per kilogram (mOsm/kg)
-12 to 14 hour fluid restriction: Greater than 850 mOsm/kg
- (265-285mmol/L)
Treatment of choice- reduce immunopathology
There is no need for alarm if kidney function tests deteriorate on the MP. This is a temporary condition. It does not mean your kidneys will fail. In most instances, terminal kidney failure develops as the result of progressive damage to the kidneys over a decade or more. Your doctor may be alarmed because doctors are taught that chronic kidney failure is an irreversible condition.
However, treatment for chronic kidney failure is dependant on treating any underlying disease. Since the cause of chronic kidney failure in Th1 diseases is inflammation, as evidenced by the waxing and waning kidney function tests with the MP antibiotics, pursuing the killing of the intracellular bacteria is essential to reverse decline in kidney function.
Adjustment of the MP meds to dampen the immune system response is the correct way to treat reduced kidney function. For details see My immune system reaction is too strong. What should I do?
To protect your kidneys from damage, increase Benicar to 40mg every 4 hours. This recent paper should help your doctor feel more confident about higher dose ARBs (Benicar):
"Long-term safety of high-dose angiotensin receptor blocker therapy in hypertensive patients with chronic kidney disease"
The FDA's package insert for Benicar notes no unusual effects on the kidneys, and gives guidance to dosing in patients with severe kidney disease (it is not precluded even in severe kidney disease). See Benicar is safe to take at the recommended MP doses
Be sure to read the following valuable information on treating elevated serum creatinine with ARBs
Print a copy of this important paper from the Department of Medicine, Division of Nephrology, University of Texas Southwestern Medical School, Dallas, TX, USA for your doctor:
"Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers: what to do if the serum creatinine and/or serum potassium concentration rises"
http://ndt.oupjournals.org/cgi/content/full/18/10/1973
This article, published in Postgraduate Medicine explains that some physicians fear ARBs will elevate creatinine levels but this is usually a problem in people who are dehydrated or who are already in later-stage kidney disease.
These articles will help Doc understand the importance of continuing the Benicar blockade:
ARBs treat chronic kidney disease
Scientific studies demonstrating Benicar is renoprotective
Effects of ARBs (as a class of drugs) on kidney function
Effects of Higher-Dose Angiotensin Receptor Blockers On Humans
Discuss these recommendations with your doctor:
- adjust antibiotics as needed to reduce immunopathology
- continue Benicar dosing for its renoprotective effects
- maintain adequate (not excessive) fluid intake
- avoid vitamin D and sunlight
- avoid excess calcium supplementation
How high can creatinine safely go?
The level of creatinine may be used as a guide to manage immunopathology. It shouldn't be necessary to keep creatinine within the normal reference range. Maintaining a level of creatinine 10-20% higher than normal indicates the kidneys are functioning adequately while the MP is inducing immunopathology to resolve kidney inflammation.
Retesting kidney function
Repeating kidney function tests every four weeks should provide adequate information. Plan the time of the date of the test for a time when immunopathology is likely to be at its lowest and make sure you are adequately hydrated to get the most positive result which will reassure Doc your kidneys are healing.
Stopping the MP
Discontinuing Benicar is not the answer. Continuing the Benicar blockade protects the kidneys from damage due to inflammation.
Stopping the MP doesn't always stop the immune system reaction. The immune system is enabled to function more efficiently with the Benicar blockade and sometimes continues to function well even if Benicar and/or antibiotics are stopped.
The decision to discontinue the MP is between you and your Doctor and your doctor may call Dr Marshall if s/he has any concerns.
Nephrocalcinosis
Nephrocalcinosis is too much calcium within the kidneys. This can impair the function of the kidneys. Nephrocalcinosis can result from sarcoidosis, vitamin D toxicity, hypercalcemia or renal tubular acidosis.
This is a temporary situation that will resolve with treatment of the underlying disease. Ultrasound is not the most reliable method of diagnosing nephrocalcinosis. Your doctor will likely want to follow up with more imaging later.
Renal disease may be exacerbated by sun exposure
Our foundation has worked hard to change the NIH's perception of sarcoidosis, but their description of kidney symptoms, for example, doesn't mention, for instance, renal failure due to a patient's sunlight exposure. For that sort of information, you need to look to the published articles indexed in PubMed - like this one which cautions sunlight exposure can lead to renal failure in some cases.
Reduce exposure to manmade toxins
It is highly likely that endotoxins are circulated via the lymphatics and vascular system to the liver and spleen and then to the elimination organs. What they are and how to measure them is at present uncertain. However, the changes in kidney and liver function tests that are seen during the Herx reaction confirm this process.
Therefore, it is important to minimize exposure to other toxins during this time especially man made toxins as they will further burden the detoxification and elimination symptoms.
-Eat as organic as possible to avoid chemical pesticides and fertilizers
-Avoid commercial and toxic household cleaning products
-Avoid breathing polluted air ~Greg Blaney, MD
Fluids and reduced kidney function
Drinking extra fluids in unlikely to affect your levels of BUN or creatinine. Maintaining adequate hydration is all that is recommended. Your doctor will tell you if you should limit fluids. See Water: How Much Should You Drink Every Day? and The Water Myth
Diet and reduced kidney function
Ask your doctor if a diet low in sodium, potassium, and phosphorous, three substances that the kidneys regulate, might be helpful in improving your kidney function.
See also Members' experiences
Related information:
Kidney disease primer
My potassium is elevated. What should I do?
My sodium is low. What should I do?
Thiazide diuretics are contraindicated in kidney disease
Benicar and kidney disease
(Scroll down for scientific studies and members' stories)
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Belinda
Research Team
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Posted: Mon Jul 31st, 2006 04:24 |
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[filelink]
ARBs treat chronic kidney disease
One of the latest treatments for chronic kidney disease is an angiotensin receptor blocker like Benicar. An ARB reduces the rate of progression of chronic kidney disease (CKD) by lowering blood pressure and proteinuria and increasing the filtering ability of the kidneys.
Temporary changes in tests such as eGFR or an increase in serum creatinine should be anticipated before beginning an ARB in CKD, but when these occur, it is an indication the ARB is working as anticipated to preserve kidney function. This article says changes in eGFR and creatinine are not an indication to stop using an ARB. These tests return to more stable numbers over time.
Studies have shown that people with CKD need higher doses of ARBs to be effective at protecting kidney function and higher doses have been well tolerated. This recent study concluded high-dose ARBs in patients with CKD did not result in any significant long-term negative effects on serum creatinine or potassium.
We also know that Olmesartan improves insulin resistance in CKD patients and lowers inflammatory markers like C-reactive protein and fibrinogen, which are trends that will help protect organ function.
You will want to discuss all these points with your doctors.
See also:
Scientific studies demonstrating Benicar is renoprotective
Effects of ARBs on kidney function
Effects of Higher-Dose Angiotensin Receptor Blockers On Humans
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Meg Mangin R.N.
Research Team
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Posted: Wed Nov 29th, 2006 23:03 |
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(filelink)
Diagnosing flank pain
Flank pain has a variety of causes. It can indicate an infection or a structural kidney problem such a stones or simply muscle spasm.
The kidneys are in the back, one on each side of the spine. They are about 2 inches (5cm) deep, just behind the lower ribs. Pain in a kidney is usually felt as upper back pain, on one side or the other. The pain can run down into the groin, or further down the back. The kidneys lie next to the muscles of the back, so that it can sometimes be difficult to tell the difference between muscle pain, back pain or kidney pain.
There are many causes of kidney pain. Infection in the kidney and kidney stones are common causes. X-ray tests will detect kidney stones. Samples of urine will be sent to the laboratory for culture tests to see if infection is present. Other conditions which cause some swelling or irritation of the kidneys may also cause pain, and these often fall into the category of "loin pain-haematuria syndrome".
Detailed medical history questions might help determine if your pain is related to your kidneys. You should feel confident that the MP will treat your pain regardless of the source.
Dr. Blaney has said he believes that much lower back pain is due to Th1 inflammation. If you are concerned, you can cut back on the antibiotics and reduce your natural light exposure to see if the symptoms calm down.
Related FAQs:
I think I have a bladder infection. What should I do?
I've developed kidney stones. What should I do?
Back pain
Members' experiences
I have been a rapid stone developer for quite a few years. They're not calcium oxalate stones so diet isn't really helpful in lessening. I have staghorn bruS***e stones.
Invariably though when ultrasounded and stones found they were not in an of themselves painful UNTIL they enter the ureter, as they start to pass. That's when it goes off the charts.
I do have flank pain regularly which I do not attribute to stones but to inflammation/disease of the kidneys. The way I can tell between stones and inflammation is the stones esculate greatly to a very high pain threshold---top of the charts, and then after passed the pain is relieved quite quickly.
But flank pain during abx tx varies from quite painful (not off the charts like trying to pass a large stone) and back down the scale to moderate or dull coinciding with breaks I have taken on the MP.
Usually it is my right kidney that hurts the most ( that has been the one that I have had infections twice a year since 13yrs old), but the left kidney with the 4+cm cyst hurts much less than the right.
At any rate the Ultrasound will give you an idea if there is any calculi present, and you may chose to ignore for now, or opt to have them pulverized. I haven't had any pulverized--and only had one hospitalization with an exceptionally large staghorn that didn't want to pass quick enough to my likings. The rest I have passed at home, catching for analysis.
I have had many stones sit in the kidney for long times though, and never give me any trouble. With the fluctuation of pain levels, I would tend to think inflammation due to another organ affected by TH1 disease. ~Hrts
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Meg Mangin R.N.
Research Team
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Posted: Mon Dec 4th, 2006 02:06 |
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(filelink)
Members experiences
-Have been to have my kidney function and BP checked and everything is much improved! Having increased my Benicar frequency to 6-hourly (and I've reduced my abx except mino to give my body a rest) my blood pressure has risen to a respectable 94/57. This is remarkable, as it had stabilized at 80/40 since I was in Phase 1. Creatinine, Urea, Urate and eGFR all returning to bearable levels. Only my anaemia remains but I will hope for that to improve slowly.
So this is a lesson to others whose doctors panic and say "woah! your BP is dropping, you should take less of that Benicar". The counter-intuitive answer is to TAKE MORE instead. ~Claudia
-My doc also worries about creatinine, but I never pushed for the 24hour test. What I did instead was to try to reduce herx, under the theory that creatinine was related to herx and both related to dying bacteria. What worked was to reduce the herx. It worked like a champ, my creatinine was normal.
What works to stop the herx seems to depend on the person and on the stage of MP. What works to convince a Doc that the Benicar isn't the problem is even more variable, but somehow you have to do it. ~Chris
-Finally my creatinine values are down in the normal range (101) (first time since I measured them in April). Hemoglobin is also up (11,5). Will slowly increase mino after having been to a nephrologist next week (only reason for seeing the specialist is to maintain a good relation to my doc). Think it is wise to keep creatinine low when I go see the specialist, so that no stopping of meds or anything will be enforced. Just finished a year on the MP, it has been a lot tougher than expected. And the time it takes seems so long. But hanging in there. ~inge 01/04/08
-I will have been off abx for 25 days. My serum creatinine is now back down to 71 umol/L (0.81 mg/dL), with an eGFR of 80 mL/min. These are the same as before starting the MP, so my GP was "relieved" when I spoke to her this morning. I haven't been able to stop smiling all day! ~Asilan
-I've had some blood tests back today and creatinine has gone down to 200. Potassium has gone down to 5.2. Urea has slightly gone down to 22.5. Haemaglobin and lymphocyte count are slightly low. So obviously slowing down the herx has helped with bloods. Bloods for me are a definite way of registering the herx because I'm always herxing and I'm not knowing the difference between tolerable and intolerable. Every since I took Benicar I found I was always herxing without the antibiotics and now I've been off Prednisilone for a year I feel like my immune reactions are very turned on and working stronger than when I started so I have found myself also dropping the antibiotic dose to cope with the herx. ~Simon Elrahi
-I received some good news during my doctor appointment. My kidney functioning tests were normal. My doctor had taken me off the MP meds back in May due to the increase in my creatinine and BUN. I wasn't sure how my tests results would be right now since I was now at the maximum doses of the MP meds. I was keeping my fingers crossed that the results would be good so my doctor wouldn't take me off the MP meds again. My doctor and I were both surprised to see that both my creatinine and BUN were normal. ~Mike9a
-Mino 25mg every two days Benicar 40mg every 3 to 5 hours. One week past kidney" crisis": New test results are almost normal. Whew. ~Somadoc
-Just to let you know, that since stopping all abx and reducing the Beni to three times a day, things are much improved- as expected they would be. Kidney function: creatinine -89 ( was 103), eGFR =62 ( was 52). ~Kas
-only benicar every 4 hours during day time and a few times once at 3 am. creatinine down from 138 to 116 (two days ago) (range 60-105). it was comforting to see that an increase in benicar did not lead to an increase in creatinine, as my nephrologist speculated it would. ~inge
-the renal bloods are so much better & the Dr will no longer blame the Benicar for the abnormal readings. During all of that time I was on the 40mg q6h Benicar, plus the occasional 20mg. The creatinin seems to be going down & the eGFR up, towards the end of the zith cycle. ~Pundun
-My eGFR was retested at 53 up from 45 which my doc informally calls a percentage. Proof that decreased light and more Benicar increase it and therefore that it is IP  . ~PatrickBurke Jul08
Last edited on Sat Jul 5th, 2008 05:49 by Meg Mangin R.N.
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Meg Mangin R.N.
Research Team
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Posted: Sat Jan 27th, 2007 03:35 |
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[filelink]
Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers: what to do if the serum creatinine and/or serum potassium concentration rises
Biff F. Palmer
Department of Medicine, Division of Nephrology, University of Texas Southwestern Medical School, Dallas, TX, USA
Correspondence and offprint requests to: Biff F. Palmer, MD, Professor of Internal Medicine, Department of Medicine, Division of Nephrology, University of Texas Southwestern Medical School, 5323 Harry Haines Boulevard, Dallas, TX 75390-8856, USA.
Keywords: angiotensin-converting enzyme inhibitors; angiotensin receptor blockers; hyperkalaemia; hypertension; serum creatinine
Introduction
Guidelines governing the optimal treatment of blood pressure in patients with chronic renal failure emphasize the need for more stringent blood pressure control and the use of drugs that interfere with the renin–angiotensin system [1,2]. As this approach is adopted, physicians will commonly encounter patients where blood pressure control is accompanied by an increase in the serum creatinine concentration and patients who develop hyperkalaemia. How physicians respond to these events is of considerable importance.
In the patient with an increase in serum creatinine concentration, decreasing the dose of antihypertensive medications and allowing blood pressure to increase will cause the serum creatinine concentration to return to the original baseline. Unfortunately, such an approach is not optimal for the long-term preservation of renal function and should be discouraged. Small and non-progressive increases in the serum creatinine concentration accompanying better blood pressure control do not reflect structural injury to the kidney but rather reflect a favourable effect on renal haemodynamics and in particular a lowering of intraglomerular pressure.
For those patients with hyperkalaemia, discontinuation of angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) therapy without first taking steps to minimize this complication is also not in the patient’s best interest given the potential cardiovascular benefits afforded by these agents. By taking several precautions, the majority of patients at risk for hyperkalaemia can be treated successfully rather than unnecessarily being labelled as intolerant to these drugs.
Blood pressure control and increases in the serum creatinine concentration
An increase in the serum creatinine concentration in the setting of better blood pressure control is seen primarily in patients with chronic renal failure. Loss of renal mass leads to disturbances in the autoregulatory ability of the remaining renal vasculature such that intraglomerular pressure begins to vary directly with changes in systemic arterial pressure [3,4]. In some patients, this impairment is severe enough that a completely pressure-passive vasculature is present where any change in mean arterial pressure is matched by a proportional change in intraglomerular pressure. Such changes explain why even modest degrees of systemic hypertension can be an important factor contributing to further renal function loss [5].
These same changes also explain why hypertensive chronic renal failure patients are more likely to develop an increase in the serum creatinine concentration when blood pressure is lowered. A blunted ability of the pre-glomerular circulation to vasodilate in response to better blood pressure control will cause an exaggerated fall in intraglomerular pressure. This change in renal function is haemodynamic in origin and does not represent structural injury to the kidney. In many patients, renal function will either improve or resolve with long-term blood pressure control, reflecting restoration of renal autoregulation back towards normal. In those patients whose renal function remains reduced, the long-term renal outcome is still improved as a result of better blood pressure control [6,7].
Renal dysfunction that accompanies antihypertensive therapy is a result of blood pressure lowering and is independent of the agent utilized. ACE inhibitors and ARBs are more commonly associated with this complication since any decline in intraglomerular pressure due to blood pressure lowering will be exaggerated by concomitant vasodilation of the efferent side of the glomerular circulation.
Consider a 52-year-old man with diabetic nephropathy and a baseline creatinine concentration of 1.8 mg/dl who on physical examination is noted to have a blood pressure of 148/92 mmHg. He is started on an ACE inhibitor, and 2 weeks later his blood pressure has fallen to 138/82 mmHg. A repeat serum creatinine concentration is now 2.2 mg/dl. Rather than discontinuing the ACE inhibitor potentially depriving this patient of an agent that can both slow the progression of his chronic renal disease and provide long-term cardiovascular protection, the appropriate response is to continue the drug and recheck laboratory values in 1 week to ensure the creatinine has stabilized at the higher value. One should not view a 20–30% increase in the serum creatinine concentration that then stabilizes as a contraindication to intensive blood pressure control or, as in this case, use of an ACE inhibitor [8].
In those situations in which the initial rise in creatinine is >30% or the repeat value shows a progressive increase, then the appropriate response is to discontinue the drug and initiate a search for other causes of renal dysfunction. There are several conditions in which use of ACE inhibitors or ARBs may cause exaggerated or progressive declines in renal function. The first setting involves significant (usually >70%) bilateral renal artery obstruction or unilateral renal artery obstruction to a solitary functioning kidney. Under these conditions, increased tone of the efferent arteriole acts to attenuate the decline in intraglomerular pressure that results from the arterial obstruction. The trade-off is that renal function and the glomerular filtration rate become dependent upon sustained constriction of the efferent vessel by angiotensin II. A similar dependence can develop in patients with polycystic kidney disease where the renal arteries become extrinsically compressed by large cysts [9]. Unless the underlying obstruction can be treated, then other classes of antihypertensive agents will have to be utilized.
ACE inhibitors and ARBs can also cause an azotaemic response under conditions of an absolute (gastroenteritis, aggressive diuresis, poor oral intake) or effective reduction in circulatory volume (moderate to severe congestive heart failure). In these settings, angiotensin II-mediated constriction of the efferent arteriole serves to minimize the decline in glomerular filtration rate that otherwise would occur as a result of the fall in renal perfusion pressure. In the volume-contracted patient, the appropriate response is to discontinue the drug and only restart it once the extracellular fluid volume has been replenished. In a patient with congestive heart failure, these drugs will increase the creatinine when the decrease in intraglomerular pressure resulting from efferent vasodilation is not offset by an increase in renal perfusion. This can occur in patients with severely depressed cardiac function in which afterload reduction can no longer increase cardiac output, or in the setting of aggressive diuresis.
A similar mechanism is responsible for renal dysfunction that occurs in patients given ACE inhibitors or ARBs in the setting of non-steroidal anti-inflammatory drugs (NSAIDs), cyclosporin A or early sepsis [10–12]. These settings are all associated with increased vasoconstriction of the renal vasculature. ACE inhibitor- or ARB-induced efferent vasodilation in the face of decreased perfusion pressure accounts for the fall in glomerular filtration rate.
Hyperkalaemia complicating the use of ACE inhibitors and ARBs
Use of ACE inhibitors or ARBs in patients with chronic renal disease can be associated with hyperkalaemia. As with a rise in the serum creatinine concentration, many physicians respond to even mild increases in the serum potassium by immediately discontinuing these drugs without first considering steps that might be taken to minimize this complication. In many instances, physicians are reluctant even to initiate such therapy simply because the patient has an elevated creatinine concentration. Such an approach is strictly to the patient’s disadvantage since patients with more advanced renal insufficiency derive a greater amount of protection from renal disease progression with these drugs [13]. While close monitoring is required, several steps can be taken to minimize the likelihood of developing hyperkalaemia.
One should review the patient’s medication profile and, wherever possible, discontinue drugs that can impair renal potassium excretion. NSAIDs, either prescribed or those taken over-the-counter, are common offenders in this regard [12]. The patients should be placed on a low potassium diet, with specific counselling against the use of potassium-containing salt substitutes. Diuretics are particularly effective in minimizing hyperkalaemia. In patients with a serum creatinine <1.8 mg/dl, thiazide diuretics can be used but, with more severe renal insufficiency, loop diuretics are required. In chronic renal failure patients with metabolic acidosis (bicarbonate concentration <20 mEq/l), sodium bicarbonate should be administered. Decreasing the dose of the ACE inhibitor or switching to one that is not totally dependent on renal excretion may be of help. In one study of patients with mild chronic renal failure, use of an ARB was found to have less of an effect on increasing serum potassium when compared with an ACE inhibitor [14]. However, this difference was small and, at present, these agents should be viewed as having similar risks for developing hyperkalaemia. Intermittent use of a potassium-binding resin can be tried; however, this drug is poorly tolerated when used on a chronic basis and has been associated with gastrointestinal ulceration [15].
With implementation of these steps, the risk of hyperkalaemia severe enough to warrant discontinuation of ACE inhibitors or ARBs is quite low even in patients with moderate to severe renal insufficiency. In patients with chronic renal disease, the serum potassium should be checked within 1–2 weeks of starting an ACE inhibitor or an ARB. If the potassium concentration increases to a value >5.6 mEq/l despite the precautions noted above, then another class of antihypertensive therapy will need to be utilized.
Conflict of interest statement. None declared.
References
- Bakris G, Williams M, Dworkin L et al. Preserving renal function in adults with hypertension and diabetes: a consensus approach. Am J Kidney Dis 2000; 36: 646–661
- American Diabetes Association. Diabetes Care 2002; 25 [Suppl 1]: S85–S89
- Bidani A, Griffin K. Long-term renal consequences of hypertension for normal and diseased kidneys. Curr Opin Nephrol Hypertens 2002; 11: 73–80
- Pelayo JC, Westcott JY. Impaired autoregulation and vulnerability to hypertensive injury in remnant nephron. J Clin Invest 1991; 88: 101–105
- Palmer BF. Impaired renal autoregulation: implications for the genesis of hypertension and hypertension-induced renal injury. Am J Med Sci 2001; 321: 388–400
- Apperloo AJ, De Zeeuw D, De Jong P. A short-term antihypertensive treatment-induced fall in glomerular filtration rate predicts long-term stability of renal function. Kidney Int 1997; 51: 793–797
- Hansen HP, Rossing P, Tarnow L, Nielsen F, Jensen B, Parving H. Increased glomerular filtration rate after withdrawal of long-term antihypertensive treatment in diabetic nephropathy. Kidney Int 1995; 47: 1726–1731
- Palmer BF. Renal dysfunction complicating treatment of hypertension. N Engl J Med 2002; 347: 1256–1261
- Chapman A, Gabow P, Schrier R. Reversible renal failure associated with angiotensin converting enzyme inhibitors in polycystic kidney disease. Ann Intern Med 1991; 15: 769–773
- Curtis JJ, Laskow DA, Jones PA, Julian BA, Gaston RS, Luke RG. Captopril-induced fall in glomerular filtration rate in cyclosporine-treated hypertensive patients. J Am Soc Nephrol 1993; 3: 1570–1574
- Schor N. Acute renal failure and the sepsis syndrome. Kidney Int 2002; 61: 764–776.
- Palmer BF. Renal complications associated with use of nonsteroidal anti-inflammatory agents. J Invest Med 1995; 43: 516–533
- Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: is this a cause for concern? Arch Intern Med 2000; 160: 685–693
- Bakris GL, Siomos M, Richardson D et al. ACE inhibition or angiotensin receptor blockade: impact on potassium in renal failure. VAL-K Study Group. Kidney Int 2000; 58: 2084–2092
- Abraham S, Bhagavan B, Lee L, Rashid A, Wu T. Upper gastrointestinal tract injury in patients receiving kayexalate (sodium polystyrene sulfonate) in sorbitol: clinical, endoscopic, and histopathologic findings. Am J Surg Pathol 2001; 25: 637–644
(Print this paper for your doctor)
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Meg Mangin R.N.
Research Team
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Posted: Sat Jan 27th, 2007 04:12 |
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(filelink)
Thiazide Diuretics are contraindicated in kidney disease
chlorothiazide (Diuril)
chlorthalidone (Hygroton)
indapamide (Lozol)
Hydrochlorothiazide (HCT, HCTZ) (Esidrix, HydroDiuril)
Persons with Th1 inflammation may have occult kidney inflammation. Thiazide diuretics are hard on the kidneys.
Please read: Paul J. Rosch: Diuretics and Diabetes
HCT is added to a lot of other combination blood pressure drugs, and these should not be used
Hydrochlorothiazide (HCT) is too hard on the kidneys and liver, and these are organs were people with Th1 disease may have undetected problems. You can read the precautions about HCT on the internet drug index.
Here are some of the HCT and HCT-containing combinations to avoid:
Accuretic
Aldactazide
Aquatensen
Aquazide
Atacand/HCT
Avalide
Benazepril/HCT
Benicar/HCT (Benicar without the HCT is the form you should take)
Bendroflumethiazide
Benicar/HCT you need the normal benicar (without the HCT)
Benzthiazide
Bisoprolol/HCT
Candesartan/HCT
Capozide
Captopril/HCT
Chlorothiazide
Diovan/HCT
Diucardin
Diuril
Dyazide
Enalapril/HCT
Enduron
Esidrix
Exna
Ezide
Fosinopril/HCT
Hydrocot
HydroDIURIL
Hydroflumethiazide
Hydromox
Hyzaar
Inderide
Irbesartan/HCT
Lisinopril/HCT
Losartan/HCT
Lotensin/HCT
Maxzide
Metahydrin
Methyclothiazide
Micardis/HCT
Microzide
Moexipril/HCT
Naqua
Naturetin
Oretic
Polythiazide
Prinzide
Propranolol/HCT
Quinapril/HCT
Quinethazone
Renese
Saluron
Spironolactone/HCT
Telmisartan/HCT
Triamterene/HCT
Trichlormethiazide
Uniretic
Valsartan/HCT
Vaseretic 10-25
Vaseretic 5-12.5
Zestoretic
Ziac
These diuretics are contraindicated because they are potassium-sparing and might result in hyperkalemia.
-spironolactone (Aldactone, Novospironton, Spiractin)
-triamterene (Dyrenium)
-amiloride (Midamor)
Lasix (furosemide) however, does not cause potassium-retention and is compatible with the MP. Anyone on Lasix with cardiorespiratory symptoms exacerbation should be evaluated by their Dr for CHF to see if their cardiac medications need to be adjusted.
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Belinda
Research Team
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Posted: Sun Sep 30th, 2007 09:29 |
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[filelink]
Scientific studies demonstrating Benicar is renoprotective
Miyata T, Takizawa S.
Toward better renoprotection: lessons from angiotensin receptor blockers.
Hemodial Int. 2007 Apr;11(2):164-8.
PMID: 17403166 [PubMed - indexed for MEDLINE]
de Vinuesa SG, Goicoechea M, Kanter J, Puerta M, Cachofeiro V, Lahera V, Gómez-Campderá F, Luño J.
Insulin Resistance, Inflammatory Biomarkers, and Adipokines in Patients with Chronic Kidney Disease: Effects of Angiotensin II Blockade.
J Am Soc Nephrol. 2006 Dec;17(12 Suppl 3):S206-12.
PMID: 17130263 [PubMed - in process]
Mizuno M, Sada T, Kato M, Fukushima Y, Terashima H, Koike H.
The effect of angiotensin II receptor blockade on an end-stage renal failure model of type 2 diabetes.
J Cardiovasc Pharmacol. 2006 Oct;48(4):135-42.
PMID: 17086090 [PubMed - indexed for MEDLINE]
Imai E, Ito S, Haneda M, Chan JC, Makino H; ORIENT Investigators.
Olmesartan reducing incidence of endstage renal disease in diabetic nephropathy trial (ORIENT): rationale and study design.
Hypertens Res. 2006 Sep;29(9):703-9
PMID: 17249526 [PubMed - indexed for MEDLINE]
Fan YY, Baba R, Nagai Y, Miyatake A, Hosomi N, Kimura S, Sun GP, Kohno M, Fujita M, Abe Y, Nishiyama A.
Augmentation of intrarenal angiotensin II levels in uninephrectomized aldosterone/salt-treated hypertensive rats; renoprotective effects of an ultrahigh dose of olmesartan.
Hypertens Res. 2006 Mar;29(3):169-78.
PMID: 16755152 [PubMed - indexed for MEDLINE]
Izuhara Y, Nangaku M, Inagi R, Tominaga N, Aizawa T, Kurokawa K, van Ypersele de Strihou C, Miyata T.
Renoprotective properties of angiotensin receptor blockers beyond blood pressure lowering.
J Am Soc Nephrol. 2005 Dec;16(12):3631-41. Epub 2005 Oct 19.
PMID: 16236804 [PubMed - indexed for MEDLINE] Full Text: http://jasn.asnjournals.org/cgi/reprint/16/12/3631
Fliser D, Wagner KK, Loos A, Tsikas D, Haller H.
Chronic angiotensin II receptor blockade reduces (intra)renal vascular resistance in patients with type 2 diabetes.
J Am Soc Nephrol. 2005 Apr;16(4):1135-40.
PMID: 15716329 [PubMed - indexed for MEDLINE]
Yoshihara K, Gao Y, Shiga H, Wada DR, Hisaoka M.
Population pharmacokinetics of olmesartan following oral administration of its prodrug, olmesartan medoxomil: in healthy volunteers and hypertensive patients.
Clin Pharmacokinet. 2005;44(12):1329-42.
PMID: 16372830 [PubMed - indexed for MEDLINE]
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Belinda
Research Team
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Posted: Sun Sep 30th, 2007 09:57 |
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[filelink]
Effects of ARBs (as a class of drugs) on Kidney Function
Studies indicate Benicar is reno-protective
Mimura T, Takenaka T, Kanno Y, Moriwaki K, Okada H, Suzuki H.
Vascular compliance is secured under angiotensin inhibition in non-diabetic chronic kidney diseases.
Hum Hypertens. 2007 Jul 26; [Epub ahead of print]
PMID: 17653243 [PubMed - as supplied by publisher]
"our data indicated that angiotensin inhibition improved patient prognosis in non-diabetic chronic kidney diseases with mild-to-moderate renal dysfunction."
Katayama S, Yagi S, Yamamoto H, Yamaguchi M, Izumida T, Noguchi Y, Inaba M, Inukai K.
Is renoprotection by angiotensin receptor blocker dependent on blood pressure?: the Saitama Medical School, Albuminuria Reduction in Diabetics with Valsartan (STAR) study.
Hypertens Res. 2007 Jun;30(6):529-33.
PMID: 17664856 [PubMed - indexed for MEDLINE]
"These results suggest that combination therapy with an ARB and CCB is very effective in lowering BP and UAE [urinary albumin excretion] in cases in which BP is not well controlled, while, even in patients with a sufficient BP control of <130/85 mmHg, the use of ARB singly resulted in a significant decrease in UAE without a further decrease in BP, implying that the ARB had a renoprotective action independent of changes in BP."
Chandar J, Abitbol C, Montané B, Zilleruelo G.
Angiotensin blockade as sole treatment for proteinuric kidney disease in children.
Nephrol Dial Transplant. 2007 May;22(5):1332-7. Epub 2007 Feb 13.
PMID: 17299000 [PubMed - indexed for MEDLINE]
"CONCLUSIONS: Angiotensin blockade alone appears to effectively control proteinuria and stabilize kidney function in children. This may provide an alternative to more toxic therapies, especially corticosteroids, in children with glomerular disorders such as those associated with obesity."
Miyata T, Takizawa S.
Toward better renoprotection: lessons from angiotensin receptor blockers.
Hemodial Int. 2007 Apr;11(2):164-8.
PMID: 17403166 [PubMed - indexed for MEDLINE]
Yu C, Gong R, Rifai A, Tolbert EM, Dworkin LD.
Long-term, high-dosage candesartan suppresses inflammation and injury in chronic kidney disease: nonhemodynamic renal protection.
J Am Soc Nephrol. 2007 Mar;18(3):750-9. Epub 2007 Feb 7.
PMID: 17287430 [PubMed - indexed for MEDLINE]
"These findings suggest that candesartan has dosage-dependent, anti-inflammatory effects that are mediated by suppression of NF-kappaB activation and chemokine expression. Renal protection with high-dosage therapy may depend on these nonhemodynamic effects."
Li Y, Takemura G, Okada H, Miyata S, Maruyama R, Esaki M, Kanamori H, Li L, Ogino A, Ohno T, Kondo T, Nakagawa M, Minatoguchi S, Fujiwara T, Fujiwara H.
Molecular signaling mediated by angiotensin II type 1A receptor blockade leading to attenuation of renal dysfunction-associated heart failure.
J Card Fail. 2007 Mar;13(2):155-62.
PMID: 17395057 [PubMed - indexed for MEDLINE]
Mahmood J, Khan F, Okada S, Kumagai N, Morioka T, Oite T.
Local delivery of angiotensin receptor blocker into the kidney ameliorates progression of experimental glomerulonephritis.
Kidney Int. 2006 Nov;70(9):1591-8. Epub 2006 Sep 20.
PMID: 16985512 [PubMed - indexed for MEDLINE]
"Local delivery of ARB into the kidney affected local RAS and thus improved the renal injury and function in the potentially progressive glomerulosclerosis of rat model."
Osawa H, Nakamura N, Shirato K, Nakamura M, Shimada M, Kumasaka R, Murakami R, Fujita T, Yamabe H, Okumura K.
Losartan, an angiotensin-II receptor antagonist, retards the progression of advanced renal insufficiency.
Tohoku J Exp Med. 2006 May;209(1):7-13.
PMID: 16636517 [PubMed - indexed for MEDLINE]
Jaggi JS, Seshan SV, McDevitt MR, Sgouros G, Hyjek E, Scheinberg DA.
Mitigation of radiation nephropathy after internal alpha-particle irradiation of kidneys.
Int J Radiat Oncol Biol Phys. 2006 Apr 1;64(5):1503-12. Epub 2006 Feb 28.
PMID: 16503385 [PubMed - indexed for MEDLINE]
Weinberg AJ, Zappe DH, Ramadugu R, Weinberg MS.
Long-term safety of high-dose angiotensin receptor blocker therapy in hypertensive patients with chronic kidney disease.
J Hypertens Suppl. 2006 Mar;24(1):S95-9.
PMID: 16601581 [PubMed - indexed for MEDLINE]
"High-dose ARB treatment in patients with chronic renal disease is not associated with any clinically significant long-term negative effects on serum creatinine or potassium and is thus a important therapeutic modality with which to achieve further reductions in urinary protein excretion."
Wang PX, Fan MQ, Huang CB, Feng JY, Xiao Y, Fang ZQ, Zhang YP.
Effect of losartan on slowing progression of chronic allograft nephropathy.
Chin Med Sci J. 2005 Dec;20(4):231-6.
PMID: 16422249 [PubMed - indexed for MEDLINE]
Zhang Z, Sun L, Wang Y, Ning G, Minto AW, Kong J, Quigg RJ, Li YC. 1Division of Biological Sciences, Department of Medicine, The University of Chicago, Chicago, Illinois, USA.
Kidney Int. 2007 Oct 10 [Epub ahead of print] Renoprotective role of the vitamin D receptor in diabetic nephropathy.
See also Kidney Disease
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Belinda
Research Team
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Posted: Sun Sep 30th, 2007 19:01 |
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[filelink]
Effects of Higher-Dose Angiotensin Receptor Blockers On Humans
These are reports on the effects of higher-dose ARBs in humans with disease.
Hollenberg NK, Parving HH, Viberti G, Remuzzi G, Ritter S, Zelenkofske S, Kandra A, Daley WL, Rocha R.
Albuminuria response to very high-dose valsartan in type 2 diabetes mellitus.
J Hypertens. 2007 Sep;25(9):1921-6.
PMID: 17762658 [PubMed - in process]
Shargorodsky M, Hass E, Boaz M, Gavish D, Zimlichman R.
High dose treatment with angiotensin II receptor blocker in patients with hypertension: Differential effect of tissue protection versus blood pressure lowering.
Atherosclerosis. 2007 Jun 21; [Epub ahead of print]
PMID: 17588581 [PubMed - as supplied by publisher]
Weinberg AJ, Zappe DH, Ramadugu R, Weinberg MS.
Long-term safety of high-dose angiotensin receptor blocker therapy in hypertensive patients with chronic kidney disease.
J Hypertens Suppl. 2006 Mar;24(1):S95-9.
PMID: 16601581 [PubMed - indexed for MEDLINE]
Schmieder RE, Klingbeil AU, Fleischmann EH, Veelken R, Delles C.
Additional antiproteinuric effect of ultrahigh dose candesartan: a double-blind, randomized, prospective study.
J Am Soc Nephrol. 2005 Oct;16(10):3038-45. Epub 2005 Aug 24
PMID: 16120821 [PubMed - indexed for MEDLINE]
Weinberg AJ, Zappe DH, Ashton M, Weinberg MS.
Safety and tolerability of high-dose angiotensin receptor blocker therapy in patients with chronic kidney disease: a pilot study.
Am J Nephrol. 2004 May-Jun;24(3):340-5. Epub 2004 Jun 10.
PMID: 15192304 [PubMed - indexed for MEDLINE]
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Belinda
Research Team
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Posted: Sun Sep 30th, 2007 19:02 |
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[filelink]
Effects of High-Dose Angiotensin Receptor Blockers On Animal Disease Models
This is a compilation of some of the reported effects of ARBs when used on animal models of disease and injury.
Yu C, Gong R, Rifai A, Tolbert EM, Dworkin LD.
Long-term, high-dosage candesartan suppresses inflammation and injury in chronic kidney disease: nonhemodynamic renal protection.
J Am Soc Nephrol. 2007 Mar;18(3):750-9. Epub 2007 Feb 7.
PMID: 17287430 [PubMed - indexed for MEDLINE]
Price A, Lockhart JC, Ferrell WR, Gsell W, McLean S, Sturrock RD.
Angiotensin II type 1 receptor as a novel therapeutic target in rheumatoid arthritis: in vivo analyses in rodent models of arthritis and ex vivo analyses in human inflammatory synovitis.
Arthritis Rheum. 2007 Feb;56(2):441-7.
PMID: 17265479 [PubMed - indexed for MEDLINE]
Fan YY, Baba R, Nagai Y, Miyatake A, Hosomi N, Kimura S, Sun GP, Kohno M, Fujita M, Abe Y, Nishiyama A.
Augmentation of intrarenal angiotensin II levels in uninephrectomized aldosterone/salt-treated hypertensive rats; renoprotective effects of an ultrahigh dose of olmesartan.
Hypertens Res. 2006 Mar;29(3):169-78.
PMID: 16755152 [PubMed - indexed for MEDLINE]
Miyata T, Yamamoto M, Izuhara Y.
From molecular footprints of disease to new therapeutic interventions in diabetic nephropathy.
Ann N Y Acad Sci. 2005 Jun;1043:740-9.
PMID: 16037301 [PubMed - indexed for MEDLINE]
Tachikawa H, Kodama M, Hui L, Yoshida T, Hayashi M, Abe S, Kashimura T, Kato K, Hanawa H, Watanabe K, Nakazawa M, Aizawa Y.
Angiotensin II type 1 receptor blocker, valsartan, prevented cardiac fibrosis in rat cardiomyopathy after autoimmune myocarditis.
J Cardiovasc Pharmacol. 2003 Jan;41 Suppl 1:S105-10.
PMID: 12688405 [PubMed - indexed for MEDLINE]
Molteni A, Moulder JE, Cohen EF, Ward WF, Fish BL, Taylor JM, Wolfe LF, Brizio-Molteni L, Veno P.
Control of radiation-induced pneumopathy and lung fibrosis by angiotensin-converting enzyme inhibitors and an angiotensin II type 1 receptor blocker.
Int J Radiat Biol. 2000 Apr;76(4):523-32.
PMID: 10815633 [PubMed - indexed for MEDLINE]
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Meg Mangin R.N.
Research Team
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Posted: Thu Jan 10th, 2008 22:35 |
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[filelink]
Vitamin D for Kidney Disease Unproven
Review of 76 Studies Shows Value of Vitamin D Treatment for Chronic Kidney Disease 'Uncertain'
By Kathleen Doheny
WebMD Medical News
Reviewed by Louise Chang, MD
Dec. 17, 2007 -- Vitamin D compounds, routinely given to patients with chronic kidney disease to help preserve their bones, are not proven scientifically to help, according to a new report.
Researchers evaluated 76 published trials on vitamin D compounds, performing what is known as a meta-analysis, in which the results of several studies are combined.
Bottom line: "Despite many years of use, this is an intervention ... of unproven efficacy when it comes to achieving what really matters -- that is, a reduction in deaths, fractures, and cardiovascular events," says Giovanni Strippoli, MD, research coordinator at the Mario Negri Sud Consortium in Italy and a co-author of the study.
The Problem
In chronic kidney disease, caused by such conditions as high blood pressure and diabetes the organs do not work properly and can eventually fail, leading to a need for dialysis.
Chronic kidney disease patients are often deficient in vitamin D, which helps maintain normal blood levels of calcium and phosphorous and helps promote calcium absorption, important for strong bones.
Diseased kidneys can't remove excess phosphorous found in foods as normal kidneys do. As phosphorous builds up, calcium in the blood drops. Then four small glands in the neck, called the parathyroid glands, become too active and too much calcium is removed from the bones, causing them to weaken and possibly fracture, according to the National Kidney Foundation.
When parathyroid hormone, as well as blood levels of phosphorous and calcium, builds up to excess, the risk of bone fractures, disability, and death increase.
To remedy the problem, doctors generally advise eating a low-phosphorous diet and taking one of a variety of medicines with a form of vitamin D and other components, either orally or injectables.
"Vitamin D compounds have been used for over 30 years and are very widespread," Suetonia Palmer, MBChB, a clinical research training fellow at the University of Otago, New Zealand, tells WebMD. "However, their effect on mortality and cardiovascular health remains unknown."
The Analysis: Vitamin D for Kidney Disease
Palmer, Strippoli and their colleagues searched medical databases from January 1966 through July 2007 to find published studies of vitamin D compounds for chronic kidney disease. They selected 76 that met their criteria for inclusion. In all, 3,667 participants were in these 76 studies.
When they pooled the results and analyzed them, the researchers found that the vitamin D compounds did not consistently reduce the parathyroid hormone levels or reduce the risk of death, bone pain, blood vessel calcification, or other problems.
When they compared the established vitamin D sterols with placebo, the vitamin D treatments were associated with a 2.3 times higher risk of high calcium levels and a nearly two times higher risk of high phosphate in the blood. And the treatment didn't consistently reduce the parathyroid hormone levels.
Newer types of vitamin D treatment did not perform better.
The analysis is published in the Annals of Internal Medicine.
Another Perspective
In an editorial accompanying the analysis, Marcello Tonelli, MD, associate professor of medicine at the University of Alberta in Edmonton, Canada, writes: "Palmer and colleagues' findings should serve as yet another warning to the nephrology community that we do not have good evidence to defend many of our common practices."
"We need to do more research," Tonelli tells WebMD. "To figure out the best role for these medicines, a large trial or trials are needed, probably funded by a U.S. government agency such as the National Institutes of Health."
He reports as a potential conflict of interest that he receives funding from the Centre for D-Receptor Activation Research to examine vitamin D status in remote-dwelling patients on dialysis.
Message for Kidney Disease Patients
Strippoli and Palmer, too, call for more research in the area to prove the treatments work.
Meanwhile, those with chronic kidney disease should follow their doctors' advice, Strippoli says. Until more is known, patients should closely follow, in particular, advice about preventive measures suggested by their doctors, including dietary advice and recommendations to undergo longer dialysis times.
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