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 Table of Contents  
Year : 2017  |  Volume : 22  |  Issue : 2  |  Page : 73-77

What we should do for chronic renal failure in India

Department of Nephrology, Apollo Hospitals, Chennai, Tamil Nadu, India

Date of Web Publication15-Sep-2017

Correspondence Address:
M K Mani
Apollo Hospitals, 21, Greams Lane, Off Greams Road, Chennai - 600 006, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jmgims.jmgims_34_17

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How to cite this article:
Mani M K. What we should do for chronic renal failure in India. J Mahatma Gandhi Inst Med Sci 2017;22:73-7

How to cite this URL:
Mani M K. What we should do for chronic renal failure in India. J Mahatma Gandhi Inst Med Sci [serial online] 2017 [cited 2021 Oct 16];22:73-7. Available from: https://www.jmgims.co.in/text.asp?2017/22/2/73/214750

We have no reliable statistics for the prevalence of chronic renal failure in India. Modi and Jha [1] estimated an annual incidence of 229 per million population, which would work out at 293,654 given our current population of 1282 million, rising every minute. My own figures from the Kidney Help Trust [2] indicate an incidence of 0.87 per 1000, which projects to 870 per million and 1,115,631 for the country. Both these studies have been done on limited populations, and we are not justified in assuming these figures for the whole country, but they give you a rough idea.

India has a small but growing number of nephrologists. Unfortunately, the attribute that sets a nephrologist apart from other physicians is that he does dialysis and runs transplant programs, and most young nephrologists feel that their mission in life is fulfilled only if they are active in these two areas. Both these lines of treatment are very expensive. While rates vary from hospital to hospital, the actual materials used in a dialysis would cost around ₹750/-, and staff charges, depreciation of the machines and the cost of the area used would add a few hundreds more. A patient needs three dialyses a week for good health and at least two for reasonable survival, so the cost of staying on dialysis would be around 1½ or 2 lakhs of rupees a year. A renal transplant would cost around ₹ 500,000/-, and maintenance immunosuppression would cost ₹ 100,000/- in the 1st year, though it might fall in later years.

The annual per capita income in India is ₹ 100,000/-, but the income distribution is grossly skewed, with the richest 10% earning 31% of the income, and the lowest 10% just 3.6%. Only 3.8% of Indians pay income tax, and all those earning more than ₹ 250,000/- are supposed to pay tax. Perhaps an equal number earn that sum but conceal it from the tax authorities, but in any case, it shows that barely 10% of Indians can afford to pay for this expensive treatment.

Could we depend on the government to pay for dialysis and transplantation? In 2015–2016, the entire government spending on health, contributed to by the center, state, and local governments, amounted to ₹ 2572/- per capita of population. In addition, the average Indian spent ₹ 6297/- per year on health. I have taken these figures from various newspaper articles on the internet and cannot vouch for their accuracy, but it is clear that they would not be far from the truth, and to speak of the average Indian, or the Central or any of the State Governments, providing dialysis or transplantation to all who need it is laughable. However, the Southern states have found it politically expedient to announce programs to provide dialysis free to all who need it. The fact is that there are not enough dialysis machines in the country to fulfill this promise, and there is no money to pay for it anyway.

In his budget for the year 2015–2016, Mr. Arun Jaitley provided funds for dialysis. His estimate was that 2.2 lakhs of people enter end-stage renal disease every year, and he meant to give them dialysis at a cost of ₹ 2000/- per dialysis. Most government programs provide eight dialyses a month or 96 dialyses a year. We would, therefore, spend 96 × 2000 × 220,000 a year, or ₹ 4224 crores in the 1st year. A reasonable program should keep patients going for at least 10 years, so at the end of 10 years, we would spend ₹ 42,240 crores on dialysis alone. Mr. Jaitley has budgeted ₹ 151,581 crores for the social sector which includes education and health care. I do not know what is the share of health in this, but it seems obvious that in 10 years our entire health budget would be spent on dialysis alone. As for the various South Indian Government programs, most private hospitals no longer accept government patients as they are not reimbursed for their expenses. There are not enough dialysis machines to take all the patients who need it, and many are put on a waiting list and die before they get their turn.

  The Prevention of Chronic Renal Disease Top

It is abundantly clear that the vast majority of Indians with end-stage renal disease will die untreated. It is so much more sensible to prevent chronic renal disease if it were feasible and affordable. The Kidney Help Trust of Chennai has established a protocol that fulfills these objectives and further has been sustained for the past 24 years. I am not citing all the papers that we have published on this subject, but they have been summarized in the paper I have mentioned.[2] Diabetes and hypertension together account for approximately half of all patients with renal failure in this country, and hypertension contributes to accelerated decline in all other diseases. Both are very common in our country. Most patients are unaware that they have the disease, as symptoms appear only when complications set in. The rural program of the trust works in 56 villages and hamlets around 50 km from Chennai and covers a population of 43,000. In a nutshell, our protocol is to screen every subject in the population every year or two during a house-to-house survey. We apply a simple questionnaire, asking for polyuria and oliguria, nocturia and dysuria, dyspnea and edema, renal angle pain, or hematuria. We record the blood pressure (BP) of the entire population and examine the urine for glucose and albumin. Everyone who tests positive on the questionnaire, the BP or the urine test undergoes a test for blood glucose and creatinine. We thereby detect all patients with hypertension and diabetes, and those who have renal disease. Renal diseases are treated as well as possible, but our main goal is to treat diabetes and hypertension effectively with the cheapest possible drugs, all provided on a domiciliary basis. We used reserpine as long as it was available, but unfortunately, this drug, which is the cheapest and the most effective antihypertensive, has been withdrawn from the market, and we now use clonidine and hydrochlorothiazide for hypertension and metformin and glibenclamide for diabetes. The trust employs one doctor and six women from the villages. We may hire four more during our surveys. We have found it easy to teach these helpers how to do the simple procedures we use, like recording of the BP, examination of the urine for glucose and protein, and maintaining the documentation we require. Once patients are identified, the doctor establishes therapy and then visits every area once a month so that every identified patient is seen by the doctor once a month. Our workers go to each area more often, check the patients, and distribute the medicines. They have made many innovations to improve the efficiency of our work such as ensuring compliance with medicines and ensuring that the patients' follow-up with the doctor. BP has been maintained below 140/90 in 96% of participants. HbA1C has been kept below 7% in 52% of diabetics and reduced by 10% or more of the original level in a further 25%. Renal failure has been brought from 28 per 1000 of the population to 11 per 1000, strokes have been reduced from 10 per 1000 to 1.8 per 1000, and “heart attacks” from 9.1 per 1000 to 2.8 per 1000. Renal failure is assessed by estimation of the glomerular filtration rate (GFR) using the Modification of Diet in Renal Disease (MDRD) formula and strokes and heart attacks by historical recall. During the surveys, participants were asked whether they or any of their family had suffered from heart attacks or strokes. Admittedly, the diagnosis of a heart attack could have been faulty in many participants, given that they are in a rural area with limited medical facilities, but a stroke is clearly identifiable by the occurrence of hemiplegia.

This program was judged by the International Society of Nephrology to be the best prevention program in the world, and I received the John Dirks Award of the society in 2005 for this work. I expected governments of the different states in India to take up similar programs through their Primary Health Centers, which are supposed to play a part in preventing disease and not just in treating established conditions. However, all my efforts to have government in my state or at the center adopt this protocol have been dismal failures. The main objection that has been raised is that we use urine examination to diagnose diabetes and would, therefore, miss a number of patients with the disease. I do not for a moment dispute that. However, random glucose measurements would be just as likely to miss the diagnosis. It would be necessary to take a definite timed blood sample, fasting or 2 h postprandial, and it is manifestly impossible to organize this in the community, besides being far more expensive. Urine is much more easily obtained and tested than a blood sample, and if we do miss a few patients in one survey, the chances are that we will pick them up on our next survey. Remember that we estimate blood glucose in all who answer any of our questions in the affirmative, who have hypertension, or who have proteinuria, in addition to those who have glycosuria. A study of 1000 patients who underwent Apollo's health check, in which we applied our methods and compared our results with the final result of the health check in the same participants (fasting and postprandial blood glucose) showed that we missed just 13.8% of the patients. The most conclusive argument is that we have prevented so much of renal failure and other complications by our cheap and sustainable methods, and any more elaborate program would be doomed to failure because it would be more costly and difficult to perform. Our cost is just ₹ 31/- per capita of the population each year including the survey, salaries of our doctor and staff, running the one van we own, and medicines. We are helped by Apollo Hospital which does the tests on our participants without charge, and we estimate the expenses as very approximately ₹ 4/- per capita of population per year. ₹ 35/- per person fits very easily into the Government's ₹ 2572/- per year per head, and the benefits are huge.

I do not expect any individual doctor to take up this kind of work, but you could help on a smaller scale, by having an assistant or a secretary, check the BP and the urine of every one of the numerous attendants who accompany each patient to your consulting room. Early diagnosis makes a great difference to the person's life. The importance of early detection and treatment has been established by the follow-up of the famous Diabetes Control and Complications Trial and Epidemiology of Diabetes Interventions and Complications trials.[3] Good control at an early stage leads to better results in the long term even if later control is not as good. Treatment can be instituted early only if we detect the disease at or soon after its onset. Active search for participants as in our program will save many lives and prevent much suffering, at a negligible cost.

  Retarding the Progression of Chronic Renal Failure Top

Prevention of renal disease in the community is the responsibility of Government and is beyond the capacity of any individual doctor. However, once a patient's renal function has fallen below normal, the onus for his care falls on us. We can delay his progression to the end stage if we make the effort. Certain general measures are obvious, but we do not give sufficient emphasis to them. Smoking and excessive body weight accelerate the decline in renal function, and we should advise our patients to stop smoking and to reduce weight. I have found it easier to get my patients to give up tobacco, but barely 5% of my patients have lost even a few kilograms despite my exhortations. Protein restriction has been established to retard progression in Western societies. The average American eats around 1.5 g of protein/kg body weight per day, most of it of animal origin. The recommended maximum is 0.8 g/kg. Only a few Indians actually consume this amount. I find most Indian doctors ask patients to stop eating dhal and pulses. I must stress that only protein of animal origin accelerates the decline in renal function. Apart from its effect on hyperfiltration, meat, fish, and milk give the patient a considerable load of phosphorus, which accelerates decline in renal function. Vegetable proteins do not cause hyperfiltration, and though they contain a lot of phosphorus, this is mainly in the form of phytates which are not absorbed from the intestines. Animal protein contributes acid radicles which have numerous harmful effects in renal failure, whereas vegetable proteins have far less. I appeal to all of you to restrict meat, fish, eggs, and milk but allow the patient to consume any amount of protein from vegetable sources. An excellent review dealing with this subject is available free on the internet,[4] and I recommend that all of you spend a few minutes to read it. Moreover, on the matter of diet, please do not deprive the poor patient of tomatoes. These have no adverse effects on the kidneys or on the patient with renal disease except for their potassium content, and they certainly do not cause renal stones.

Another common practice among Indian nephrologists and physicians is to prescribe two to six tablets of keto-analogs of essential amino acids. The scientifically proved benefit of these agents applies only to patients maintained on a very low protein diet (0.3 g/kg/day) supplemented by keto-analogs, and the dose of keto-analogs required amounts to around 24 tablets a day. It has been widely reported that this combination slows decline in renal function compared to a low protein diet (0.8 g/kg/day), but the effect has never been found to be very great. Follow-up of patients in the MDRD study has raised some doubts about this.[5] The authors found that the very low protein diet did not retard progression of renal failure and also increased the risk of death. They discuss whether this is due to the very low protein intake or to some harmful effects of the keto-analogs. In the absence of clear evidence of benefit, coupled with the possibility of harm, added to the fact that this is an expensive tablet, I think we would be better off avoiding keto-analogs, restricting animal protein, and allowing unrestricted intake of vegetable proteins.

One other unscientific practice in India is the prescription of tablets containing n-acetyl cysteine for patients with chronic renal disease. There is not an iota of evidence for this. A PubMed search for articles with the terms chronic kidney disease and acetyl cysteine in the title or abstract yielded eight articles, dealing with various experiments on different kinds of cells. There is not one clinical paper to suggest a benefit to patients. A brilliant manufacturer thought of a name for the tablet suggesting that kidneys would somehow be protected by these tablets, and a number of others produced tablets with similar composition and names, and the Indian medical profession has fallen for this. We could save our patients considerable expense by avoiding these tablets too.

The acidosis of chronic kidney disease could lead to muscle wasting, bone disease, inflammation, faster progression, and greater mortality. Acidosis is less likely on a vegetarian diet. In addition, if the serum bicarbonate is below 23 mEq/L, it would be advisable to correct acidosis by the administration of sodium bicarbonate.[6]

Uric acid levels are also associated with accelerated progression [7] and increased mortality.[8] There is some evidence that lowering serum uric acid levels to 6 mg/dL with febuxostat or allopurinol may have benefit, but this is not conclusive. Febuxostat has fewer risks of  Stevens-Johnson syndrome More Details and may be preferable.

The undisputed methods that work to retard the progression of renal failure are control of BP and reduction of proteinuria.[9] Normally protein gets absorbed by endocytosis into the proximal tubule cell through megalin and gets digested in the lysosomes, the constituent amino acids being returned to the body. When the load is excessive in patients with significant albuminuria, intracellular reactions are set off which can lead to apoptosis of the tubular epithelial cell and to inflammatory, vasoactive, and fibrotic reactions leading to chronic interstitial changes accelerating the decline in renal function. Angiotensin-converting enzyme inhibitors (ACEi) and angiotensin receptor blockers reduce proteinuria by hemodynamic effects and direct effects on the podocytes.[10] The dose should be built up to the maximum possible, as long as there is an incremental reduction in the quantity of protein leaking in the urine. There is no point in increasing the dose if there is no effect.

One of the limiting factors in building up ACEi is the antihypertensive effect. If BP falls too low, you cannot increase the dose of ACEi or angiotensin receptor blockers (ARBs). In this situation, I recommend that you add a small dose of indomethacin. Nonsteroidal anti-inflammatory drugs reduce proteinuria by reducing glomerular filtration, and they increase the BP. Just as for ACE inhibition, you must monitor renal function and potassium while gradually increasing the dose, to guard against renal failure. When the BP comes up, you can increase the dose of the ACEi.

There is no doubt that tight control of BP reduces the rate of decline in renal function. There has been considerable debate on how low we should go, with many people advocating that BP should not be lowered below 140/90. The debate has probably been laid to rest by the SPRINT trial,[11] which compared an intensive treatment group whose systolic BP was lowered to a mean of 121.4 mmHg with a standard treatment group whose mean systolic BP was 136.2. The primary composite outcome was myocardial infarction, other acute coronary syndromes, stroke, heart failure, or death from cardiovascular causes. The study was stopped after a median period of 3.26 years because the primary outcome was lower in the intensive group (1.65% per year vs. 2.19%) and so was all cause mortality (155 intensive, 210 standard, and hazard ratio 0.73). The answer is clear. Bring the blood pressure to the lowest, the patient can tolerate without troublesome orthostatic hypotension or features of end-organ ischemia. I would add a word of caution. Coronary artery filling occurs during diastole, so it is advisable to keep diastolic pressure at or above 70 mmHg in participants at risk of coronary disease.

It is universally accepted that control of BP retards the progression of renal failure. There is no consensus on the level to be attained or the agents that should be used. Majority opinion favors ACEi or angiotensin receptor blockers,[12] but there are a few vociferous opponents to their use.

On the basis of various trials, the recommendation now is not to use ACEi and ARBs in combination.[13],[14] However, even Bakris [13] accepts that the combination may be useful in patients with massive proteinuria. Recent discovery of details of an intrarenal renin-angiotensin system [15] suggests, first, that renin-angiotensin-aldosterone system inhibition is an important target in treating these patients and second that much larger doses may be required than was previously thought. The major problem with randomized controlled trials is that they use fixed combinations of different drugs, and patients are allocated at random to the different groups. This eliminates the most vital part of medical practice, personalized attention to the patient. The objection to combinations is that more adverse effects are seen in the form of hyperkalemia and accelerated renal failure. In an extensive experience over several decades, I have eliminated the harmful effects of combinations and retained the benefits, by the simple expedient of starting with one category, building up the dose carefully with constant monitoring, achieving the maximum benefit possible with that drug, measured by the reduction of BP and albuminuria, and then adding a drug from the other category and increasing to the maximum effective dose with similar monitoring and assessment. If BP control is inadequate even with this dose, other agents must be added for BP control is vital. The methodology I use is published in detail.[16],[17] For easier access to Indian readers, the paper from seminars Seminars was reprinted with permission in Postgraduate Medicine. In a nutshell, patients are started on low doses of enalapril or losartan (the cheapest drugs in their class). They monitor BP, serum creatinine, and serum potassium in their own locality and communicate the results to me by E-mail, and I increase the dose in stages. If there is too rapid a rise in azotemia or potassium levels, or if the BP falls too low, the drugs can be withdrawn or the dose reduced. Once the maximum benefit in the reduction of BP or of proteinuria is achieved, the other drug (losartan or enalapril) is added and the dose similarly increased to the maximum effective and safe level. If BP is not controlled even with the maximum dose, any other agent (usually cilnidipine) is added, and BP is brought to 130/80 or less. A refinement I have added after these publications is to monitor the rate of decline at the different dose levels. After a few years, one can pick out the dose at which the decline in renal function was the least, and that dose may be maintained for the long term. With these measures, the rate of decline of renal function has been brought from a loss of GFR of 8.6 ml/min/year in diabetic nephropathy to 2.5 ml/min/year, in chronic glomerulonephritis from 5.8 to 2.6, in chronic interstitial nephritis from 3.4 to 1.2, and so on in all diseases. In the total of some thousands of patients with chronic renal failure of all causes, the decline is reduced from an average of 5.7 ml/min/year to 2 ml/min/year. If patients with all renal diseases are detected as soon as their GFR falls below normal and put on appropriate therapy, we can give them an astonishing prolongation of life before they reach the end stage from 15 years without such intensive therapy to 40 years, which means that most of them will attain their normal life span without need for dialysis or transplantation. I must stress that this involves some of the doctor's time, maybe around 5 min after each personal consultation to tabulate and calculate the rate of decline in the interval between visits, and a few minutes to answer every letter from each patient. If ever you feel that this is too much time to spend, I would ask you whether 5 min of your time is worth more than 25 years of your patient's life.

Not every patient is prepared to take the trouble to do the necessary tests and write letters. Many will come only once a year and the dose is increased only when they come to me. They serve as my control group, and they suffer in consequence of their indolence, needing dialysis and transplantation early. We can do no more than persuade. Unfortunately, we do not have the power to enforce our advice.

Very few other nephrologists follow these practices. However, I have company from a very famous group in Italy who also follow similar methods and achieve similar results.[18]

We need to do the best we can to maintain hemoglobin at ideal levels (10–12 g/dL) for the maximum comfort of the patient and to minimize cardiac changes. This is easily achieved with the use of erythropoietin, but I must express two limitations. Please keep hemoglobin levels below 12 g/dL. Mortality has been found to be higher with levels above this. If hemoglobin does not rise with your treatment, look for other causes of anemia such as iron deficiency and correct them. Once this is eliminated, please remember to raise erythropoietin dose till hemoglobin rises. There is no point in continuing an ineffective dose as it just costs money while providing no benefit. Furthermore, there are limits above which one must accept that there is a resistance to erythropoietin, and we should not push the dose further.

My major objection is that most of us do not explain to the patient that there is no such thing as a course of erythropoietin. This drug will work as long as it is administered. When you stop it, the hemoglobin will fall back to the original level. Make sure your patient understands this and the financial implications of life long therapy before you write your prescription. Patients adapt to the anemia and most do not feel the effects. A normal hemoglobin does not retard the progression of renal failure, and ultimately your patient must find the resources to pay for dialysis or transplantation. If all his money is used up in keeping his hemoglobin high, even one who might have been able to afford dialysis and transplantation might have to give up his life.

We should also keep patients free from mineral bone disease with the appropriate use of Vitamin D analogs and phosphate binders.

My ambition is to see that every Indian should stay free from renal failure, and those whose renal function falls in spite of our efforts should be maintained on efficient conservative management so that he lives his full life span without ever needing renal replacement therapy. I appeal to all of you to join me in this effort.

  References Top

Modi GK, Jha V. The incidence of end-stage renal disease in India: A population-based study. Kidney Int 2006;70:2131-3.  Back to cited text no. 1
Mani MK. A glimmer of hope for prevention. Natl Med J India 2010;23:109-10.  Back to cited text no. 2
Nathan DM; DCCT/EDIC Research Group. The diabetes control and complications trial/epidemiology of diabetes interventions and complications study at 30 years: Overview. Diabetes Care 2014;37:9-16.  Back to cited text no. 3
Snelson M, Clarke RE, Coughlan MT. Stirring the pot: Can dietary modification alleviate the burden of CKD? Nutrients 2017;9. pii: E265.   Back to cited text no. 4
Menon V, Kopple JD, Wang X, Beck GJ, Collins AJ, Kusek JW, et al. Effect of a very low-protein diet on outcomes: Long-term follow-up of the Modification of Diet in Renal Disease (MDRD) Study. Am J Kidney Dis 2009;53:208-17.  Back to cited text no. 5
Kraut JA, Madias NE. Metabolic Acidosis of CKD: An Update. Am J Kidney Dis 2016;67:307-17.  Back to cited text no. 6
Johnson RJ, Nakagawa T, Jalal D, Sánchez-Lozada LG, Kang DH, Ritz E. Uric acid and chronic kidney disease: Which is chasing which? Nephrol Dial Transplant 2013;28:2221-8.  Back to cited text no. 7
Xia X, Luo Q, Li B, Lin Z, Yu X, Huang F. Serum uric acid and mortality in chronic kidney disease: A systematic review and meta-analysis. Metabolism 2016;65:1326-41.  Back to cited text no. 8
Lambers Heerspink HJ, Gansevoort RT. Albuminuria is an appropriate therapeutic target in patients with CKD: The pro view. Clin J Am Soc Nephrol 2015;10:1079-88.  Back to cited text no. 9
Márquez E, Riera M, Pascual J, Soler MJ. Renin-angiotensin system within the diabetic podocyte. Am J Physiol Renal Physiol 2015;308:F1-10.  Back to cited text no. 10
SPRINT Research Group, Wright JT Jr., Williamson JD, Whelton PK, Snyder JK, Sink KM, et al. A Randomized Trial of Intensive versus Standard Blood-Pressure Control. N Engl J Med 2015;373:2103-16.  Back to cited text no. 11
James PA, Oparil S, Carter BL, Cushman WC, Dennison-Himmelfarb C, Handler J, et al. 2014 evidence-based guideline for the management of high blood pressure in adults: Report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA 2014;311:507-20.  Back to cited text no. 12
Bakris GL. Dual RAAS blockade is desirable in kidney disease: Con. Kidney Int 2010;78:546-9.  Back to cited text no. 13
Tobe SW, Clase CM, Gao P, McQueen M, Grosshennig A, Wang X, et al. Cardiovascular and renal outcomes with telmisartan, ramipril, or both in people at high renal risk: Results from the ONTARGET and TRANSCEND studies. Circulation 2011;123:1098-107.  Back to cited text no. 14
Navar LG. The intrarenal renin-angiotensin system in hypertension. Kidney Int 2004;65:1522-32.  Back to cited text no. 15
Mani MK. Treating renal disease in India's poor: The art of the possible. Semin Nephrol 2010;30:74-80. Reprinted Post graduate Medicine Vol 25. Delhi. Indian College of Physicians 2011; 240 – 246.  Back to cited text no. 16
Limesh M, Annigeri RA, Mani MK, Kowdle PC, Rao BS, Balasubramanian S, et al. Retarding the progression of chronic kidney disease with renin angiotensin system blockade. Indian J Nephrol 2012;22:108-15.  Back to cited text no. 17
  [Full text]  
Gentile G, Remuzzi G, Ruggenenti P. Dual renin-angiotensin system blockade for nephroprotection: Still under scrutiny. Nephron 2015;129:39-41.  Back to cited text no. 18

  Authors Top

Dr. M.K. Mani, pioneer in Nephrology in our country, and Chief Nephrologist, Apollo Hospital, Chennai, India, and Managing Trustee of Kidney Help Trust, Chennai, India, has proved to the world that it is possible to prevent chronic renal failure at a community level with a very limited budget. True to the maxim, "The smallest good deed is better than the grandest good intention," the rural program of the Kidney Help Trust envisioned by Dr. M.K. Mani has been instrumental inpreventing around 60% of chronic renal failure in a small rural community in Sriperumbudur Taluk, about 50 kms from Chennai. Dr. Mani is the recipient of many awards, including the Padma Bhushan and the Rabindranath Tagore Award, John H. Dirks Award, International Society of Nephrology in 2005, D Sc (Honoris Causa), The Tamilnadu Dr. M.G.R. Medical University in 2004., D Sc (Honoris Causa), NTR University of Health Sciences in 1999. and the Dhanvantari Award, 2011. He says-"It would be wonderful if all of us are motivated by a burning desire to relieve human suffering".

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