RENAL DATA FROM ASIA-AFRICA
|Year : 2011 | Volume
| Issue : 5 | Page : 1064-1071
|End-stage renal disease in Nigeria: An overview of the epidemiology and the pathogenetic mechanisms
MO Odubanjo1, CA Okolo1, AO Oluwasola1, A Arije2
1 Department of Pathology, Department of Internal Medicine, University College Hospital, Ibadan, Nigeria
2 Department of Nephrology Unit, Department of Internal Medicine, University College Hospital, Ibadan, Nigeria
Click here for correspondence address and email
|Date of Web Publication||6-Sep-2011|
| Abstract|| |
There is paucity of information on the magnitude of the burden of renal disease in our environment. Obtaining accurate data is hampered by the poor socioeconomic status of most patients with lack of access to specialized care in tertiary institutions, where most of the data is generated. The incidence of chronic renal failure (CRF) and end-stage renal disease (ESRD) in any specified area is known to be influenced by the prevalence of specific disease entities resulting in CRF. Hypertension, glomerulonephritis (GN), sickle cell disease, quartan malaria nephropathy, urinary tract schistosomiasis and other parasite-related forms of chronic GN are known to contribute significantly to the incidence of CRF in Nigeria. As is the situation in other parts of the world, diabetic nephropathy appears to be of increasing importance in the causation of ESRD in Nigeria. Even though the underlying cause of renal disease can often not be treated, extensive studies in experimental animals and preliminary studies in humans suggest that progression in chronic renal disease may largely be due to secondary factors, attention to which may be important in the prevention and/or control of renal disease.
|How to cite this article:|
Odubanjo M O, Okolo C A, Oluwasola A O, Arije A. End-stage renal disease in Nigeria: An overview of the epidemiology and the pathogenetic mechanisms. Saudi J Kidney Dis Transpl 2011;22:1064-71
|How to cite this URL:|
Odubanjo M O, Okolo C A, Oluwasola A O, Arije A. End-stage renal disease in Nigeria: An overview of the epidemiology and the pathogenetic mechanisms. Saudi J Kidney Dis Transpl [serial online] 2011 [cited 2022 May 22];22:1064-71. Available from: https://www.sjkdt.org/text.asp?2011/22/5/1064/84571
| Introduction|| |
The pattern of renal disease in any region or country is mainly determined by environmental factors. In general, genetic factors are known to play a less important role. In Nigeria, the role of sickle cell disease in renal disease and other genetic factors affecting susceptibility to malaria [an important cause of chronic glomerulonephritis (GN)] such as the sickle cell trait, glucose6-phosphate dehydrogenase (G6PD) deficiency variant A-, and certain genes affecting immune processes, are of epidemiological importance. 
It is generally accepted that the spectrum of renal disease in the tropics is essentially the same as in the temperate environment, but the priority determinants, the natural history of renal disease and factors in its etiopathogenesis vary among different parts of the tropics.  The data on which these observations are based however, are largely from specialized tertiary health institutions and may not be entirely representative of the pattern of distribution in the general population.
It is the progression of chronic renal failure (CRF) that leads to end-stage renal disease (ESRD). According to the Kidney Disease Outcomes Quality Initiative of the National Kidney Foundation,  ESRD is said to be present when the glomerular filtration rate (GFR) has fallen below 15 mL/min/1.73m 2 or if a patient requires renal replacement therapy (RRT) at higher GFR levels.
Although exceptions abound, the evolution from normal renal function to symptomatic CRF progresses through five stages defined based on measured or estimated GFR.  The suffixes p, T and D are added to the stage to indicate that there is significant proteinuria, patient has a renal transplant and patient is on dialysis, respectively.
| Epidemiology of End-Stage Renal Disease|| |
End-stage renal disease is the final event of a sequence that begins with an initial insult and progresses towards total loss of renal function. The incidence of CRF and ESRD in any specified area may be influenced by the prevalence of specific disease entities resulting in CRF and by the availability of funds, sophisticated modalities of treatment and expertise required in the care of the varied types of renal diseases. 
While data on the epidemiology of ESRD in the developed nations of the world abound, there is paucity of information on the magnitude of the burden of renal disease in our environment. ,,,,,, Internationally, the United States Renal Data System (USRDS), the Australian and New Zealand Dialysis and Transplant Registry (ANZDATA), the Canadian Organ Replacement Register (CORR), the European Renal Association/European Dialysis and Transplant Association (ERA-EDTA) Registry, the Japanese Registry and the relatively new Latin American Registry, are all valuable sources of data on the trends in the epidemiology of ESRD.  Nine countries participate in the ERA-EDTA registry (Austria, Belgium, Denmark, Finland, Greece, The Netherlands, Norway, Spain, UK (Scotland). 
The incidence and the prevalence of ESRD are good indicators of the burden of renal disease in a country. The prevalence is influenced by the number of new patients and the number of deaths (patient mortality). In our environment, the poor socioeconomic status of most patients with renal disease precludes access to care in the teaching hospitals where most of the data is generated. Naicker  had also expressed similar concern about the likelihood of gross underestimation of the burden of ESRD. She observed that the statistics of the South African Dialysis and Transplant Registry (SADTR) reflect the patients selected for RRT and do not accurately reflect the etiology of CRF as public sector state facilities will offer RRT only to patients who are eligible for a transplant.
In the year 2000, a total of 1764 people commenced RRT in Australia (a rate of 92 pmp) and 417 people (107 pmp) in New Zealand. The Australian and New Zealand rates are substantially lower than in the USA (311 pmp) and Japan (240 pmp) but similar to the rates reported from England (89 pmp) and most European countries.  When similar values from 1981-1991  are considered, obvious trends observed include a consistent increase in incidence and prevalence rates, particularly in older patients and in patients with diabetes mellitus.  The USRDS 1994 report shows significantly lower incidence rates than those documented for 2000, but a similar distribution was seen in the US and Japan at 200 and 180 pmp respectively. Canada, Australia, the US white-only population and most European countries had treated incidence rates between 20 and 100 pmp.  Prevalence counts and rates also show a similar distribution by being highest in the US and in Japan. 
Recent reports show that growth in incident rates pmp has slowed significantly, with the annual percent change less than one percent in 2000 and 2001. Incidence and prevalence counts and rates of patients with diabetes have continued to rise, but not as sharply in recent years, and the rate of growth in incident rates of diabetic ESRD has also slowed. Incident rates for patients with a primary diagnosis of GN have declined slightly since the mid-1990s. 
In Nigeria, as stated earlier, the actual incidence and prevalence of ESRD is not clearly known . The prevalence of CRF has been shown in various parts of Nigeria to be 1.6%,  10%,  8%,  6.7%,  and 3.6%.  Akinsola et al,  suggested that the wide variation in the values from various studies appears to be due to variations in the sources of the data consulted.
Several studies from Nigeria have shown that the peak incidence of ESRD in Nigeria is between the third and fifth decades of life. ,,,,,, In the US, the peak incidence is between the ages of 45 and 64 years. 
Naicker  observed that Nigeria is not alone in the lack of accurate figures for the burden of ESRD and states that there are no reliable statistics for ESRD in all African countries. Some authors ,, have expressed the opinion that ESRD is likely to be more prevalent in Africa than has been described in the developed countries of the world. Naicker observed that renal disease, especially glomerular disease, is more prevalent in Africa and seems to be of a more severe form than that found in Western countries.
Some authors , have attributed the increased prevalence of chronic renal disease in our environment to the impact of hypertension and GN on the population. Hypertension is known to play an important role in chronic kidney disease, which may result from, or result in renal disease. Hypertension in CRF is very common and contributes to morbidity and mortality by accelerating the progression of chronic kidney disease.  About 85% of patients with ESRD have hypertension,  which is in part responsible for the high incidence of cardiovascular events and deaths in these patients.  Chronic GN, mostly resulting from infectious causes, is also known to be an important cause of ESRD in Nigeria.
In a six-year study of 3632 patients with ESRD, based on SADTR statistics, hypertension was reported to be the cause of ESRD in 4.3% of whites, 34.6% of blacks, 20.9% of mixed-race group and 13.8% of Indians. Malignant hypertension is an important cause of morbidity and mortality among urban black South Africans, with hypertension accounting for 16% of all hospital admissions (Naicker S, 2003). Hypertension affects about 20% of the adult population (Naicker S). The influence of racial differences on the incidence of ESRD and the increased prevalence of hypertension and ESRD among African-Americans had been documented by several authors including Arikan and Tegular  and Rostand. 
In the US, diabetes is especially common among Native Americans (63.2%) and, to a lesser extent, Asians/Pacific Islanders (41.6%). Hypertension is notably common among blacks (35.9%) and GN is disproportionately common among Asian-Pacific Islanders (17.8%) in whom, it is seen twice as frequently as in black patients. 
The causes of ESRD in North America and in many developed countries are diabetes and hypertension, which together account for almost 60% of dialysis patients. In comparison, the common causes of CKD/ESRD in Nigerian adults have been documented in several studies to be hypertension, chronic GN and chronic pyelonephritis. ,,, In the recent past, the emergence of diabetes mellitus as an increasingly common cause has been documented by Alebiosu et al,  in a study where diabetes was found to be the third commonest cause of ESRD and constituted 28.4% of cases. A worldwide increase in the prevalence of diabetes as a cause of ESRD is well documented.  This increase continues to occur in spite of low protein diets, blood pressure control, and the use of angiotensin-converting enzyme (ACE) inhibitors. It is unclear why the rate of diabetic nephropathy continues to increase even when adjusted for age, gender, and race, while the incidence rates for non-diabetic ESRD remain steady. Reasons suggested for this increase include advancing obesity, carbohydrate intolerance and insulin resistance. 
Studies from Nigeria have shown the commonest cause of ESRD in Nigerian children to be glomerulopathies followed by urological abnormalities, most commonly posterior urethral valves. ,,
There are also variations in the causes of ESRD among various age-groups in America. In the US, in the peak incidence age-group (45-64 years), diabetes is the most common cause of ESRD, followed by hypertension and GN. Less common causes include interstitial nephritis, vasculitis, cystic diseases and urological diseases. A few cases are due to unknown causes in persons younger than 20 years; common primary renal diseases are GN, cystic, hereditary and congenital diseases. In this age-group, diabetes is rare. In persons older than 64 years, the most common causes of ESRD are hypertension (36.8%) and diabetes (35.9%). Diabetes is relatively more common in women and hypertension is relatively more common in men.  There are about one million people alive with ESRD in the world today just because they have access to one form or another of RRT. As expected, 90% of them live in the developed countries.  Since 1990, the number of patients on hemodialysis has almost doubled and the number of patients with transplants has increased more than 90% in the US. Peritoneal dialysis has also increased, although this modality still accounts for only 13.5% of the ESRD population. Racial differences are evident in the distribution of treatment modalities among both the incident and prevalent populations. Between 1994 and 1998, the greatest percentage increase in the number of hemodialysis patients occurred among the Native Americans and Asian populations, 11.2%, 8.5%, respectively. Compared to white patients, a lower percentage of minority patients received transplants, and these patients were more likely than white patients to be on hemodialysis.  In Nigeria, there is limited access to RRT. Most patients who are able to access treatment will have peritoneal dialysis or hemodialysis. Funding remains a problem and there is need to develop more prevention programs and make RRT more accessible. , A study showed that 70.8% of the subjects could afford dialysis for less than one month while only 1.9% could afford to continue dialysis for over 12 months.  Renal transplantation has been commenced in the last few years and is available at a few tertiary centers including the University College Hospital, Ibadan; the Obafemi Awolowo University Teaching Hospital, Ile-Ife and at a private facility in Lagos, Nigeria. Poverty, inadequate facilities and lack of donors are major problems facing kidney transplantation in our society.  There is need for health ducation to improve attitudes towards kidney donation. 
The lack of access to RRT is the main reason for the high mortality rates seen in ESRD patients in Nigeria. Abdurraham  documented a mortality rate of 54% in children with CRF. Other reasons for the high mortality include late presentation of patients to the hospitals , and the increased prevalence of steroid-resistant nephrotic syndrome in children.
| Etiopathogenesis|| |
End-stage renal disease is the final common end-point for various causes of CRF. The geographical variations in the distribution of the underlying causes of ESRD have been alluded to earlier. The peculiar features of CRF in the tropical environment have been highlighted by several authors like Hutt, Akinkugbe and Kadiri in independent articles. ,, Noteworthy is a relatively higher prevalence of chronic GN (CGN) in developing tropical countries than in the developed ones. This is due to a variety of infective agents including plasmodium malariae, filarial worms, hepatitis B virus, schistosoma mansoni, mycobacterium leprae and streptococcal organisms which are present in endemic proportions in the tropics. 
Pathogenesis of end-stage renal disease
The pathogenesis of renal damage in various disease conditions has been well-elucidated in various texts. Whatever the origin of the chronic renal disease process, be it a primary glomerular, tubular, interstitial or vascular disease, there is tendency for it to ultimately destroy all the four components of the kidney, thus culminating in ESRD kidneys.
Although the underlying problem often cannot be treated, extensive studies in experimental animals and preliminary studies in humans suggest that progression in chronic renal disease may largely be due to secondary factors that are unrelated to the activity of the initial disease.  The identification of the role of these secondary factors is important clinically because they can be treated with a view to preventing or at least minimizing further renal injury.
The roles of dietary protein restriction in the management of proteinuria and that of antihypertensive therapy for systemic and intra-glomerular hypertension have been most widely studied.
The major histological manifestation of these secondary causes of renal injury is focal and segmental glomerulosclerosis. 
Intra-glomerular hypertension and glomerular hypertrophy
An increase in intra-glomerular pressure (intra-glomerular hypertension) resulting in glomerular hyperfiltration has been demonstrated in progressive renal failure. A compensatory increase in glomerular size (glomerular hypertrophy) may also occur. The increase in intra-glomerular pressure may result from the transmission of systemic pressures or occur via glomerular-specific processes and it may have deleterious long-term effects. At least three factors contribute to the increase in intra-glomerular pressure: ,
The mechanisms by which glomerular hypertension and hypertrophy induce glomerular injury are incompletely understood. Multiple factors may be involved. These include: direct endothelial damage, increased wall stress and increased glomerular diameter with resultant deposition of hyaline material in the sub-endothelial space, narrowing of the capillary lumen and subsequent decrease in glomerular perfusion and filtration and increased strain on the mesangial cells resulting in the production of cytokines and more extracellular matrix.
- A compensatory response to nephron loss in an attempt to maintain the total glomerular filtration rate,
- Primary renal vasodilatation, as occurs in diabetes mellitus and other disorders,
- In glomerular diseases, a compensatory adaptation to a reduction in glomerular capillary permeability which is ultimately detrimental. 
It has been suggested that proteinuria itself may contribute to disease progression. Proposed mechanisms include mesangial toxicity, tubular overload and toxicity from specific filtered proteins such as transferrin/iron and induction of pro-inflammatory molecules such as monocyte chemo-attractant protein-1. ,,
All forms of CRF are associated with marked tubulointerstitial injury (tubular dilatation, interstitial fibrosis), even if the primary process is a glomerulopathy. , The degree of tubulointerstitial disease is a better predictor of the glomerular filtration rate and long-term prognosis than the severity of glomerular damage in almost all chronic progressive glomerular diseases. It is postulated that tubulointerstitial disease causes tubular atrophy and/or obstruction, eventually leading to nephron loss but the mechanism is incompletely understood. ,,
Hyperlipidemia is common in patients with chronic renal disease, particularly patients with the nephrotic syndrome. It has been shown experimentally, for example that hyperlipidemia activates the mesangial cells (which have LDL receptors), leading to stimulation of mesangial cell proliferation and to increased production of macrophage chemotactic factors, fibronectin and reactive oxygen species. ,, Each of these changes can contribute to glomerular injury.
Hyperphosphatemia in chronic renal diseases may contribute to the progression of disease, partly by phosphate precipitation along with calcium in the renal interstitium.  The calcium phosphate salt may then initiate an inflammatory reaction, resulting in interstitial fibrosis and tubular atrophy thereby worsening the chronic kidney disease.
Altered prostanoid metabolism
Glomerular prostaglandin production (PGI2 , PGE1, PGE2 and PGD2 ) tends to be increased in glomerular disease. This response may represent an appropriate intra-nephronal adaptation, since the ensuing renal vasodilatation helps to maintain the GFR in the presence of an often marked reduction in glomerular capillary permeability induced by the underlying disease. , This renal vasodilatation results in increased intra-glomerular pressure and has deleterious long-term effects.
Metabolic acidosis and decreased ammonium production
As the number of functioning nephrons declines, each remaining nephron excretes more acid (primarily as ammonia). The local accumulation of ammonia can directly activate complement, leading to secondary tubulointerstitial damage demonstrable, at least, in experimental animals. 
Progressive anemia, due largely to erythropoietin deficiency is a common complication of advanced renal disease. Experimental studies suggest that this may be a protective adaptation, since anemia leads to reduced vascular resistance which lowers both systemic blood pressure and intra-glomerular pressure. 
Dialysis of non-uremic animals with glomerulosclerosis preserves the glomerular filtration rate and slows the rate of further glomerular damage.  This observation suggests that retention of ultrafiltrable toxins during the course of progressive renal disease contributes to secondary glomerular injury. The exact mechanism by which retained toxins contribute to renal injury is not clearly known.
Filtration of normally non-filtered iron-transferrin complex with subsequent dissociation of this complex in the tubular lumen leads to the release of free iron which can promote tubular injury by promoting the formation of hydroxyl radicals (ferrous form, Fe2+ → Fenton reaction). 
Increased production of corticosteroids may accelerate the progression of renal failure. , A study assessing the efficacy of inhibiting endogenous cortisol synthesis in patients with diverse causes of CRF showed that this prevented progression in some, but not all the patients. There is need for the assessment of the role of this approach in a controlled fashion in a larger number of patients.
The decrease in renal function in an experimental model of kidney failure, the rat remnant kidney model, is accompanied by a reduced level of the vasodilator nitric oxide, which may be required for normal renal function. The administration of arginine, the amino acid precursor to nitric oxide, ameliorated the renal dysfunction possibly by increasing the levels of nitric oxide. A randomized double-blind controlled study, however, failed to show any benefit after six months of the administration of L-arginine supplementation to patients with CRF. 
In conclusion, further human studies are needed to determine the role of early and effective management of some of these secondary hemodynamic and metabolic derangements in the preservation of renal function as well as the prevention of renal failure and/or its progression.
| References|| |
|1.||Luzzatto L. Genetic factors in malaria, Bulletin of the World Health Organization 1974,50, pp195-202 |
|2.||Hutt MS. Renal disease in a tropical environment, Transactions of The Royal Society of Tropical Medicine and Hygiene, 1980;74:17-21. |
|3.||CKD Guidelines: KDOQI clinical practice guidelines on chronic kidney disease; evaluation, classification, and stratification. Kidney Disease Outcome Quality Initiatives (KDOQI) Am J Kidney Dis 2002;39(2 Suppl. 1):246-51. |
|4.||Asinobi AO. Chronic Renal Failure in Childhood. Dokita 1995; 22:76-82. |
|5.||Naicker S. End-stage renal disease in sub-Saharan and South Africa. Kidney Int Suppl 2003;83:S119-22. |
|6.||Oyediran, AB, Akinkugbe OO. Chronic renal railure in Nigeria. Trop Geog Med 1970;22:41- 5. |
|7.||Ojogwu LI, The pathologic basis of end-stage renal disease in nigerians: experience from Benin city. West Afr J Med 1990;9:193-6. |
|8.||Ojogwu LI, Anah CO. Renal failure and hypertension in Tropical Africa - a pre-dialysis experience from Nigeria. E Afr Med J 1983;60:478-84. |
|9.||Mabayoje MO, Bamgboye EL, Odutola TA, Mabadeje AF. Chronic renal failure at the Lagos University Teaching Hospital: A 10 year review. Transplant Proc 1992;24:1851-2. |
|10.||Akinkugbe OO. Nephrology in a tropical setting. Nephron 1978; 22: 249-52. |
|11.||Ruggenenti P, Schieppati A, Remuzzi G. Progression, remission, regression of chronic renal diseases. Lancet 2001:357:1601-08. |
|12.||Arýkan H, Tuðlular S.The growýng global burden of end stage renal dýsease (ESRD). Marmara Med J 2005;18(3):143-50. |
|13.||1994 Annual data report. Chapter XII International Comparisons of ESRD Therapy United States Renal Data System (USRDS) Registry 1994. |
|14.||2003 Annual data report. United States Renal Data System Registry (USRDS) 2003. |
|15.||Akinsola W, Odesanmi WO, Ogunniyi JO, Ladipo GO. Diseases causing chronic renal failure in Nigerians-a prospective study of 100 cases. Afr J Med med Sci 1989;18:131-7. |
|16.||Kadiri S, Arije A. Temporal variations and meteorological factors in hospital admissions of chronic renal failure in South West Nigeria. WAJM 1999;18:49-51. |
|17.||Alebiosu CO, Ayodele OO, Abbas A, Olutoyin A. Chronic renal failure at the Olabisi Onabanjo university teaching hospital, Sagamu, Nigeria. Afr Health Sci 2006;6(3):132-8. |
|18.||Ojo OS, Akinsola AA, Nwosu SO, Odesanmi WO. The pathological basis of chronic renal failure in Nigerians. West Afr J Med. 1990 Jul-Sep;9(3):193-6. |
|19.||Salako BL, Kadiri S, Etok V, Adesola K. The clinical and laboratory evaluation of patients with chronic renal failure in UCH Ibadan before their first dialysis. Dokita 1995;22(1):56-9. |
|20.||Arije A, Kadiri S, Akinkugbe OO. The viability of hemodialysis as a treatment option for renal failure in a developing economy. Afr J Med Med Sci 2000;29(3-4):311-4. |
|21.||Alebiosu CO. An update on progression promoters in chronic renal disease. J Natl Med Assoc USA 2003;95:30-42. |
|22.||Rostand SG, Kirk K A, Rutsky EA, Pate BA. Racial differences in the incidence of treatment for end stage renal disease, N Engl J Med 1982; 306(21):1276-9. |
|23.||Alebiosu CO. Clinical diabetic nephropathy in a tropical African population. West Afr J Med 2003;22(2):152-5. |
|24.||Abdurraham MB, Onuora CU, Babaoye FA, Narayana PT. Renal failure in children in Northern Nieria. East Afr Med J 1983:60(7); 472-7. |
|25.||Anochie I, Eke F. Chronic renal failure in children: a report from Port Harcourt, Nigeria (1985-2000). Pediatr Nephrol 2003;18:692-5. |
|26.||Arogundade FA, Barsoum RS. CKD prevention in Sub-Saharan Africa: a call for governmental, non-governmental, and community support. Am J Kidney Dis 2008;51(3):515-23. |
|27.||Bamgboye EL. End-stage renal disease in sub-Saharan Africa. Ethn Dis 2006;16(2 Suppl 2): S2-5-9. |
|28.||Badmus TA, Arogundade FA, Sanusi AA, et al. Kidney transplantation in a developing economy: challenges and initial report of three cases at Ile Ife. Cent Afr J Med 2005;51(9-10):102-6. |
|29.||Aghanwa HS, Akinsola A, Akinola DO, Makanjuola RO. Attitudes towards kidney donation, J Natl Med Assoc 2003;95(8):725-31. |
|30.||UpToDate, Copyright 2000 by McGraw-Hill Companies Inc. (Burton D. Rose - Founder and Editor in Chief), Vol. 6 No. 2. |
|31.||Rennke HG. How does glomerular epithelial call injury contribute to progressive glomerular damage? Kidney Int Suppl 1994; 45:558. |
|32.||Rennke HG, Anderson S. Brenner BM. Structural and functional correlations in the progression of renal disease in: Tisher CC, Brenner BM (Eds), Renal Pathology, Lippincott Philadelphia, 1989, PP 43-66. |
|33.||Ting RH, Kristal B, Nyers BD. The biophysical basis of hypofiltration in nephritic humans with membranous nephropathy. Kidney Int 1994;45: 390. |
|34.||Burton C, Harris KP. The role of proteinuria in the progression of chronic renal failure. Am J Kidney Dis 1996;27:765. |
|35.||Eddy AA, McCulloch L. Liu E, Adams J. A relationship between proteinuria and active tubulointerstitial diseases in rats with experimental nephritic syndrome. Am J Pathol 1991; 138:1111. |
|36.||Wang Y, Chen J. Chen L, et al. Induction of monocyte chemoattractant protein-1 in proximal tubule cells by urinary protein. J Am Soc Nephrol 1997;8:1537. |
|37.||Ong AC, Fine LG. Loss of glomerular function and tubulointerstitial fibrosis: Cause or effect. Kidney Int 1994;45:345. |
|38.||Nath KD. Tubulointerstitial changes as a major determinant in the progression of renal damage. Am J Kidney Dis 1992;20:1. |
|39.||Alexopoulos E, Seron D, Hartley RB, Cameron JS. Lupus nephritis: Correlation of interstitial cells with glomerular function. Kidney Int 1990; 37:100. |
|40.||Lan HY, Patterson DJ, Atkins RC. Initiation and evolution of interstitial leukocyte infiltration in experimental glomerulonephritis. Kidney Int 1999;56:1751. |
|41.||Hill PA, Lan HY, Nikolic-Paterson DJ, Atkins RC. Intercellular adhesion molecule-1 directs migration and localization of interstitial leukocytes in experimental glomerulonephritis. Kidney Int 1994;45:32. |
|42.||Keane WF. Lipids and the kidney. Kidney Int 1994;46:910. |
|43.||Rovin BH, Tan LC. LDL Stimulates mesangial fibronectin production and chemo attractant protein 1 expression. Kidney Int 1993;43:218. |
|44.||Kean WF, O'Dannell MP, Kasiske BL, Kim Y. Oxidative modification of low-density lipoproteins by mesangial cells. J Am Soc Nephrol 1993;4:187. |
|45.||Loghman-Adham M. Role of phosphate retention in the progression of renal failure. J Lab Clin Med 1993;122:16. |
|46.||Takahashi K, Schreiner GF, Yamashita K, et al. Predominant functional roles for thromoboxane A2 and prostaglandin E2 during late nephrotoxic serum glomerulonephritis in the rat. J Clin Invest 1990;85:1974. |
|47.||Nath KA, Hostetter MK, Hostetter TH. Pathophysiology of chronic tubulo-interstitial disease in rats. Interraction of dietary acid load, ammonia and complement C3. J Clin Invest 1985;76: 667. |
|48.||Lafferty HM, Anderson S, Brenner BM. Anaemia, a potent modulator of renal hemodynamics in models of progressive renal disease. Am J Kidney Dis 1991;17:2. |
|49.||Motojima M, Nishijima F, Ikoma M, et al. Role for "Uremic toxin" in the progressive loss of intact nephrons in chronic renal failure. Kidney Int 1991;40:461. |
|50.||Alfrey AC, Fromen DH, Hammond WS. Role of iron in the tubulo-interstitial injury in nephotoxic serum nephritis. Kidney Int 1989;36:753. |
|51.||Walser M. Progression of chronic renal failure in man. Kidney Int 1990; 37: 1195. |
|52.||Walser M, Hill S. Effect of ketoconazole plus low-dose prednisolone on progression of chronic renal failure. Am J Kidney Dis 1997;29:503. |
|53.||Reyes AA, Purkirson ML, Karl I, Klahi S. Dietary supplementation with L-arginine ameliorates glomerular hypertension in rats with sub-total nephrectomy. J Am Soc Nephrol 1994;4: 1690. |
A O Oluwasola
Department of Pathology, University College Hospital, Ibadan, Oyo State
Source of Support: None, Conflict of Interest: None
|This article has been cited by|
||Population genetics of chronic kidney disease: The evolving story of APOL1
| ||Wasser, W.G. and Tzur, S. and Wolday, D. and Adu, D. and Baumstein, D. and Rosset, S. and Skorecki, K. |
| ||Journal of Nephrology. 2012; 25(5): 603-618 |
| Article Access Statistics|
| Viewed||7065 |
| Printed||108 |
| Emailed||0 |
| PDF Downloaded||1097 |
| Comments ||[Add] |
| Cited by others ||1 |