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ACUTE RENAL FAILURE
Year : 1994  |  Volume : 40  |  Issue : 3  |  Page : 118-9

Some aspects of acute renal failure in the tropics.


Department of Pathology, Christian Medical College & Hospital, Vellore, India., India

Correspondence Address:
A Date
Department of Pathology, Christian Medical College & Hospital, Vellore, India.
India
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Source of Support: None, Conflict of Interest: None


PMID: 0008699374

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Keywords: Adult, Child, Child, Preschool, Human, Incidence, India, epidemiology,Kidney Failure, Acute, epidemiology,etiology,Risk Factors, Tropical Climate,


How to cite this article:
Date A. Some aspects of acute renal failure in the tropics. J Postgrad Med 1994;40:118

How to cite this URL:
Date A. Some aspects of acute renal failure in the tropics. J Postgrad Med [serial online] 1994 [cited 2019 Nov 13];40:118. Available from: http://www.jpgmonline.com/text.asp?1994/40/3/118/546




'The word 'tropics' is more than a geographical expression. It evokes a variety of images, including the one that it is home for most of humankind. However, this presentation will confine itself to that part of the tropical world as seen in a large South Indian Hospital. The choice of details is governed by the special interests of the author and the need to avoid topics to be covered by other speakers at this meeting.

In children, acute renal failure (ARF) accounts for about 15% of all cases admitted for investigation and treatment of medical (that is, non-urological) renal disease. A third of the cases of ARF are due to the haemolytic uraemic syndrome (HUS) complicating bacillary dysentery, and particularly those resulting from infections caused by  Shigella dysenteriae Scientific Name Search e serotype[1]. The frequency of HUS varies depending upon the waxing and waning of the prevalence of this organism, as a cause of bacillary dysentery; for example it has been quite uncommon during the last few years.

About a quarter of the cases of ARF are due to glomerulonephritis. Acute gastroenteritis and septicemia account for about 20%. Rarer causes include cholera, snake bite and nephrotoxins such as diethylene glycol, mercuric chloride and sulphonamides.

The lesions of HUS are believed to be due to Shiga toxin (Verotoxin), which damages cell membranes including that of the endothelium. This activates the coagulation mechanism, resulting in thrombocytopaenia, fragmentation of erythrocytes causing anaemia and schistocytosis, and thrombosis in renal blood vessels producing a variety of ischaemic lesions and ARF. Even in a single biopsy, glomeruli showing the following different lesions can often be identified:

(1) Intraglomerular coagulation with deposition of platelets and fibrin products in the capillary lumen and subendothelial space produces a solid avascular glomerulus, seen on light microscopy.

(2) Activation of fibrinolytic mechanisms results in unblocking of the capillary lumen but subendothelially deposited products & coagulation remain, producing the characteristic electron microscopic feature of a widened subendothelial space filled with fine granular debris. These glomeruli on light microscopy appear relatively normal, except for some 'smudging' of capillary walls.

(3) Thrombosis of the afferent vasculature of glomeruli could cause the isolated infarcted glomeruli stuffed with blood that are such a characteristic light microscopic feature of biopsies from patients with the HUS. On electron microscopy such glomeruli show necrosis of cells leaving bare glomerular capillary basement membranes and degenerating erythrocytes. As these latter'are cleared, the basement membranes collapse and the glomerulus is apparently resorbed.

(4) When larger arcuate or intralobular vessels are occluded, frank cortical necrosis occurs. This can vary in extent, but is usually patchy making prognostication on biopsy appearances unreliable.

Some long-term survivors may develop a glomerulonephritic illness. Glomerulonephritis presenting as ARF is usually an acute proliferative or crescentic, very often with serological evidence of streptococcal infection, and of the immune complex type. Antiglornerular basement membrane antibody disease is quite rare, accounting for less than 10% of cases of crescentic glomerulonephritis. One unusual feature of acute proliferative glomerulonephritis in our patients, is the large number of eosinophilic leukocytes that are sometimes present along with the usual neutrophils. This is related to blood eosinophil levels and is a reflection of the high prevalence of intestinal helminthiasis, filarisis and scabies in the population.

In adults, of all cases of medical renal disease requiring a biopsy, about 10% present as ARF. This excludes cases of ARF following surgery that are not biopsied. More than 60% of cases of ARF have acute tubular necrosis, 12% have cortical necrosis, 6% have interstitial nephritis and 19% have glomerulonephritis.

Obstetrical problems are the major cause of cortical necrosis giving rise to 70% of cases. Russell's viper bite is not uncommon, in certain rural regions of south India, and it can result in acute tubular necrosis and less frequently cortical necrosis. Allopathic and indigenous medicines are another frequent cause of ARF especially in the elderly.

In regard to interstitial nephritis, it should be kept in mind that eosinophilic leukoeytes are often seen in the renal interstitium in a variety of unrelated conditions, in tropical populations, and their presence is therefore not as strong a predictor of drug allergies, as in the developed world. Also, granulomatous interstitial nephritis seen commonly as a reaction to drugs in the Western countries, is most often the result of tuberculosis in the tropics.

This survey has emphasised the exotic causes of ARF; that is, those conditions that are either not present in the Western developed part of the world, or have been eradicated from it. They include post-streptococcal glomerulonephritis with or without crescents, HUS due to Shigellosis and snakebite. It also indicates factors in the life style of the majority of the population of tropical countries, that give rise to ARF including, poor sanitation and contaminated water that causes Shigellosis and gastroenteritis; an inadequate health care structure, especially for obstetric care, accounting for most cases of cortical necrosis; and also the uncontrolled sate and use of allopathic and indigenous medicines.

The tropics are also the home of large numbers of poor disadvantaged and malnourished people, in whom severe bacterial infections are an important cause of death. These unfortunate people have autopsy findings rarely seen in the Western developed world during the last half century. For example, in a study of autopsies of patients with leprosy, non leprous bacterial infections were present in more than 85% of cases and were a major cause of death in more than 40%. Many cases with severe infections had secondary renal lesions capable of causing ARF. These included multiple renal abscesses, intravascular coagulation and acute tubular necrosis.

As we enter the 21st century, it is possible that many of the socio-economic factors promoting ARF will, to a certain extent, be mitigated, but this gain is likely to be offset by the coming epidemic of AIDS, which will bring its own set of causes of ARF including, disseminated viral, bacterial, fungal and protozoal infections and the powerful, but nephrotoxic, chemotherapeutic agents required for combating these.

Most of the data used in the above presentation have been published in the series of papers given below. These publications can be consulted for more detail.

 
 :: References Top

1. Date A, Jacob M, Johny KV. Eosinophilic leucocytes in diffuse proliferative and exudative glomerulonephritis. Am J of Trop Mod & Hygiene 1977; 26:1028-1031.  Back to cited text no. 1    
2.Raghupathy P, Date A, Shastry JCM, Sudarsanam A, Jadhav M. Hemolytic Uremic Syndrome complicating Shigella Dysentery in South Indian children. Br Mod J 1978; 1:1518- 1521.  Back to cited text no. 2    
3.Date A, Raghupathy P, Shastry JCM. Nephron Injury in the Hemolytic Uremic Syndrome complicating Bacillary Dysentery. Journal of Pathology 1981; 133:1-16.  Back to cited text no. 3    
4.Raghupathy P, Data A, Shastry JCM, Jadhav M, Pereira SM. Acute Renal Failure in South Indian children; a ten year experience. Annals of Tropical Paediatrics 1981; 1:39-44.  Back to cited text no. 4    
5.Date A, Raghupathy P, Jidhav M, Pereira SM, Shastry JCM. Outcome of the Hemolytic Uremic Syndrome complicating Bacillary Dysentery. Annals of Tropical Paediatrics 1982; 2:1-6.  Back to cited text no. 5    
6.Date A, Unni JC, Raghuypathy P, Jadhav M, Pereira SM, Richard J, Jacob CK, Kirubakaran MG, Shastry JCM, editors. The patttern of Medical Renal Disease in children in a South Indian Hospital. Annals of Tropical Paediatrics 1984; 4:207-211.  Back to cited text no. 6    
7.Date A, Hariharan S, Jayavarthini SE. Renal lesions and other major findigs in necropsies of 133 patients with leprosy. Int J of Leprosy 1985; 53:455-460.  Back to cited text no. 7    
8.Unni JC, Date A, Raghupathy P, Shastry JCM. Medical Renal Disease in South Indian infants. Acta Paediatrica Scandinavia 1986; 75:1030-1031.  Back to cited text no. 8    
9.Date A, Raghavan R, John TJ, Richard J, Kirubakaran MG, Shastry JCM. Renal Disease in adult Indians: A clinicopathological study of 2827 patients. Quart J of Mod 1987; 64:729-737.  Back to cited text no. 9    
10.Hariharan S, Date A, Kirubakaran MG, Shastry JCM. Medical Renal Disease in the Elderly in a South Indian Hospital. Nephron 1988; 49:119-121.  Back to cited text no. 10    
11.Date A, Jeyaseelan L, Brahmadathan KN. Changing pattern of Primary Glomerulonephrifls in a South Indian Hospital. Transactions of the Royal Society of Tropical Medicine & Hygiene 1989; 83:419-40.   Back to cited text no. 11    




 

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2004 - Journal of Postgraduate Medicine
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