|Year : 2000 | Volume
| Issue : 1 | Page : 1-12
|Renal Complications of the Human Immunodeficiency Virus Infection
Tejinder S Ahuja, Mahendra Agraharkar
Department of Internal Medicine, Division of Nephrology, The University of Texas Medical Branch at Galveston, Texas, USA
Click here for correspondence address and email
|How to cite this article:|
Ahuja TS, Agraharkar M. Renal Complications of the Human Immunodeficiency Virus Infection. Saudi J Kidney Dis Transpl 2000;11:1-12
The prevalence of acute and chronic renal failure is high in patients with human immunodeficiency virus (HIV)-infection. Higher predisposition for infections with sepsis, volume depletion and nephrotoxicity due to drug therapy are the major causes of acute renal failure. Chronic renal failure, on the other hand, results from a distinct type of focal and segmental glomerulosclerosis (FSGS) termed HIV-associated nephropathy (HIVAN), and occurs mainly in blacks. However other glomerular diseases such as IgA nephropathy, membranoproliferative glomerulonephritis (related to concomitant infection with hepatitis C) and membranous glomerulonephritis can also result in renal insufficiency in patients with HIV-infection.
|How to cite this URL:|
Ahuja TS, Agraharkar M. Renal Complications of the Human Immunodeficiency Virus Infection. Saudi J Kidney Dis Transpl [serial online] 2000 [cited 2021 Aug 4];11:1-12. Available from: https://www.sjkdt.org/text.asp?2000/11/1/1/36684
It is unclear whether these glomerular diseases are coincidental or if there is a direct causative relationship with HIVinfection. In this review we will discuss renal complications of HIV-infection which either occur with higher frequency in or are unique to, patients with HIV-infection. These complications are divided into three categories: HIV-associated nephropathy; acute renal failure and electrolyte abnormalities.
HIV-associated nephropathy (HIVAN) is characterized by rapidly progressive focal and segmental glomerulosclerosis (FSGS) having distinct clinical and morphologic features. It was first reported in 1984 by investigators from Brooklyn and Miami in the United States. , After initial skepticism about the entity from West Coast researchers from the United States (US) who were mainly following HIV-1 infected white homo-sexuals, HIVAN became recognized as a distinct disease entity predominantly affec-ting blacks. This racial preponderance is not only seen in adults but also in children who have acquired the disease from perinatal infection. The reasons for this strong racial predisposition for HIVAN are unclear, but the same genetic factors, which account for higher prevalence of diabetic nephropathy, hypertensive nephrosclerosis and focal segmental glomerulosclerosis in blacks are likely to be responsible. Human leukocyte antigen (HLA) associations similar to that seen in idiopathic FSGS may increase the risk of HIVAN. 
Although intravenous drug abuse (IVDA) and male sex are considered as other risk factors, the disease can occur in the absence of drug abuse and in females. Bourgoignie et al, and others have reported on HIVAN in the Haitian community in whom the prevalence of intravenous drug is uncommon.  Although the prevalence of HIVAN varies depending upon the demographics of the population studied, initial studies suggested that approximately 10% of HIV-infected patients develop HIVAN. ,,,,,,, Winston et al. based on incidence rate of HIVAN in New York have predicted that by the end of the decade, HIVAN will be the third common cause for end-stage renal disease among young black patients.  However, studies from some other centers have not reported a similar frequency of HIVAN. Cantor et al, found only 53 patients with renal disease among 330 HIV infected patients treated at their hospital.  Fourteen of these patients had chronic renal failure and FSGS was seen in only 43% of these patients on renal biopsy.  Similarly, some autopsy studies have found HIVAN as an uncommon lesion on examination of renal tissue. ,,,,,, A lower proportion of blacks in many of these studies could have accounted for low prevalence of HIVAN. At our institution we screened 557 HIV-1 infected patients followed in the HIV-clinic for HIVAN to determine the true prevalence of HIVAN. Fifty percent of these patients were black. The overall prevalence of HIVAN in our study was 1.8%, however, as all of our patients with HIVAN were black, the prevalence of HIVAN in them was 3.5%.  Various factors could have accounted for lower prevalence of HIVAN in our study. In many of the initial studies, only the patients referred for nephrology consultation or hospitalized patients were evaluated for HIVAN, in contrast to a general HIV-1 infected population in our study. In some other studies only patients with acquired immunodeficiency syndrome (AIDS) and renal failure were included. It is also possible that with decreasing morbidity and mortality from HIVinfection, due to potent anti-retroviral therapy, the incidence of HIVAN is also decreasing. Furthermore, incidence and prevalence studies need to be conducted to provide more information regarding changing trends of HIVAN in HIV-1 infected patients.
Marked proteinuria and rapid decline in renal function resulting in end-stage renal disease (ESRD) characterize HIVAN. The mean protein excretion was 6.6 g/24 hours in 26 patients described by Rao et al,  Renal survival after the onset of HIVAN is poor and majority of patients develops ESRD in less than six months from the time of diagnosis. , In the eight patients we studied, the mean time to ESRD from the time of renal biopsy was 62.6 ± 19 days.  However, the progression of renal failure in children with HIVAN is less dramatic. , Unlike other causes of nephrotic syndrome leading to renal insufficiency, hypertension, frequent in patients with HIVAN for unclear reasons. Hypertension (diastolic BP > 100) was present only in 40% of patients in one series, but has been far less prevalent in several other published reports. , All our patients with HIVAN had normal blood pressure (<140/90), despite the fact that none of them were taking any antihypertensive drugs. The renal ultrasound reveals enlarged echogenic kidneys in the majority of patients with HIVAN. The mean size of each kidney was 12.3 cm despite that most of the patients had reached ESRD. , Marked interstitial infiltrate with cystic dilatation of the tubules is likely responsible for enlarged kidneys.
The characteristic features of HIVAN on light microscopy are focal segmental glomerulo-scelrosis with collapse of the glomerular tuft [Figure - 1]. Collapse is defined as retraction and wrinkling of the basement membrane leading to occlusion of glomerular capil-laries. Another striking component of the HIVAN is marked hypertrophy and hyper-plasia of visceral epithelial cells almost forming pseudocrescents in some cases [Figure - 2]. These cells may also reveal large nuclei and intracytoplasmic resorption droplets. The cystic enlargement of the tubules containing proteinaceous casts with marked tubulointerstial infiltrate is cons-picuous in majority of the cases [Figure - 3].
The casts usually contain albumin and immunoglobulin. On immunofluorescence, IgM, C3, and less frequently C1 is seen in areas of glomerulosclerosis as well as mesangium of the nonsclerotic glomeruli. Although immune complex glomerulonephritis has been reported in some centers, it is less common in the US. Tubuloreticular inclusions also referred to as "interferon footprints" are detected within glomerular and vascular endothelial cells in over 90% of biopsies, with HIVAN. However, we have observed these in only 20% of our patients. This difference could represent the changing histology of renal biopsies with better antiretroviral therapy. These tubulo-reticular inclusions can also be seen in patients with lupus nephritis. On electron microscopy the reticular inclusions are localized to dilated cisternae of endoplasmic reticulum. 
The direct cytopathic effect of HIV on renal cells has not been established. Although one study has shown the presence of virus in the tubular cells by in situ hybridization using cDNA probes and immuno-stains for p24 antigen, these results have not been con-firmed by others. Moreover immunostaining for viral antigens in formalin fixed paraffin embedded tissue is unreliable. In addition, the virus cannot infect tubular cells in vitro, where as glomerular endothelial cells and mesangial cells in vitro can be infected with the virus. , The evidence for the presence of the virus in the same cells in vivo is conflicting due to the technical difficulties. Kimmel et al, by using microdissection techniques on renal biopsies have detected HIV genome in glomerular, tubular and interstitial cells by polymerase chain reaction (PCR) of HIV viral genes. 
The HIV genome was detected in renal tissue irrespective of the type of glomerular disease, these results even if accurate only suggest that direct viral infection of the kidneys may be common, but is not enough to cause nephropathy and other factors may be necessary. It is likely that infiltrating mononuclear cells infected with virus produce certain cytokines, especially TGF-β, which can not only lead to fibrogenic changes in the kidney but can also, increase replication of the virus. The development of the transgenic mouse model for HIVAN is helpful in the understanding of the HIV nephropathy, however only three of the eight founders of heterozygous transgenic mice developed nephropathy resembling HIVAN. In addition, viral RNA was detected only in early stages prior to development of nephropathy and became undetectable after 60 days. Rev proteins were the only virally encoded proteins that could be identified in the glomeruli. It is not clear whether this was from endogenous synthesis or trapping in the course of glomerular filtration. These findings suggest that productive virus in the kidney may not be necessary to produce nephropathy. ,,, HIVAN can develop at any stage of HIV-1 infection irrespective of the viral load.  Therefore exact causative role of the HIV-1 virus in the pathogenesis of HIVAN is far from established.
A wide spectrum of renal disease can be seen in patients with HIV-1 infection [Table - 1]. Nephrotic range proteinuria is not only the result of HIVAN in patients with HIVinfection but can also result from IgA nephropathy, membranoproliferative glomerulonephritis (associated with concomitant infection with Hepatitis C), membranous glomerulonephritis, minimal change glomerulonephritis, amyloidosis and fibrillary glomerulonephritis.  Although heroin neph ropathy can cause focal segmental glomerulosclerosis, the collapse of glomerular tuft, tubuloreticular inclusions and cystic dilatation of the tubules are not seen with the same frequency as in HIVAN. Kidneys are usually small and contracted in heroin nephropathy in contrast to enlarged echogenic kidneys seen in patients with HIVAN.  A collapsing form of FSGS can also occur in the absence of HIV infection called idiopathic collapsing FSGS (IFSGS). 
We found in a comparative analysis, that the mean arterial pressure, mean serum cholesterol and serum albumin were higher in patients with IFSGS compared to HIVAN but the progression of renal failure was faster in patients with HIVAN.  However, every patient with collapsing FSGS should be checked for HIV-infection and disease should be termed HIVAN in seropositive patients. An extremely varied renal pathology in HIV-infected patient underscores the importance of renal biopsy for accurate diagnosis and appropriate management.
As no randomized controlled trials have been carried out in patients with HIVAN, the optimal treatment of the disease is unknown. However, antiretroviral therapy, angiotensin converting enzyme inhibitors and immuno-suppressive therapy have been tried. 
A number of reports exist in the literature on resolution of proteinuria from HIVAN after antiretroviral therapy azidothymidine (AZT). It has been suggested that AZT may also retard the progression of renal failure.  Although the role of newer antiretroviral drugs in treatment of HIVAN has not been studied, aggressive antiretroviral therapy in patients with HIVAN has shown to improve overall survival.
Kimmel et al, in a case control study compared nine patients with biopsy proven HIVAN to nine patients with HIVAN treated with captopril.  The renal survival was better in treated patients (156 ± 71days) compared to control patients (37 ± 5 days). Burns et al, in a nonrandomized prospective study evaluated 20 patients with HIVAN. Of the 11 patients with nonnephrotic proteinuria, seven were treated with fosi-nopril, and of the nine patients with nephrotic syndrome, five were treated with fosinopril. Untreated patients served as controls. At 12 weeks, the serum creatinine of treated and non-treated patients with nephrotic syndrome was 2.0 ± 1 and 9.2 ± 2 mg/dl, respectively (P=0.02). The beneficial effect extended further as at 24 weeks serum creatinine of treated and untreated patients with non nephrotic proteinuria was 1.5 ± 3.4 and 4.9 ± 2.4 mg/dl, respectively (P=0.006).  Therefore, angiotensin converting enzyme inhibitors appear to have similar renoprotective effects in HIVAN as in other renal diseases.
Smith et al treated four patients who had HIVAN with corticosteroids. Serum creatinine of all the patients decreased significantly, however the proteinuria did not change. Un-fortunately, two of the patients developed mycobacterium avium intracellulare (MAI) infection.  They later extended their expe-rience to include another 16 patients. Only 17 of the 20 patients had biopsy proven HIVAN and 19 of the 20 patients in the study were black. Of the 19 patients with renal insufficiency treated with cortico steroids 17 showed a decrease in serum creatinine concentration. Mean serum creatinine improved from 8.1 ± 1.2 to 3.0 ± 0.4 mg/dl (P<0.001). The mean time to reach a nadir of serum creatinine con-centration was five weeks. Twelve patients also had a reduction in their level of urinary protein excretion, from a 9.1 ± 1.8 to 3.2 ± .6 g/day (P<0.005). However, a large number (52%) either relapsed after a period of 20 weeks or developed new opportunistic infections (31.5%).  Randomized, placebo controlled studies are thus needed to answer whether treatment with corticosteroids leads to higher complication rate or a diminution in the rapidity of the rate of progression to ESRD.
The experience with use of cyclosporine in HIVAN is limited. In three HIV-infected pediatric patients with HIVAN, cyclosporine induced remission was obtained in all patients. The longest remission was one year in one of these patients. However, relapse occurred in all patients on discontinuing the treatment. 
In 1980 the prognosis of HIV-infected patients on dialysis was dismal and it was an ethical dilemma whether these patients should be offered renal replacement therapy. However, recent reports have suggested that survival has markedly improved and the stage of the HIV infection is the major predictor of the survival. The factors responsible for improved survival are potent antiretroviral therapy, better management of opportunistic infections, and adequate dialysis delivery. 
Patients can either choose peritoneal dialysis (PD) or hemodialysis (HD). Although there is a theoretical possibility that hemodialysis may stimulate replication of the virus due to stimulation of leukocytes and macrophages leading to release of cytokines, which upregulate expression of HIV, this effect was not observed by us. In contrast, we found that there was a small reduction in viral load after dialysis, which could have been due to adsorption of the virus to the dialysis membrane, as no virus was detected in the ultrafiltrate.  Despite the improving survival, morbidity and mortality still remains high in HIV-infected HD patients. The patients on HD have more access related problems and a higher rate of peritonitis is seen in patients on peritoneal dialysis.
As per National Kidney Foundation-National Institutes of Health task force: asymptomatic HIV-1 infected patients should not be denied consideration for transplantation and that transplantation should continue to be a treatment option for HIVinfected ESRD patients until it has been clearly established to be contraindicated. Although long-term survival has been reported in patients with HIV infection and organ transplantation, some studies have suggested faster progression to AIDS. ,
Presently in the US, solid organ transplant is not done if the patient is HIV-infected, but this is likely to change as survival of these patients continue to improve with better antiretroviral therapy.
Acute Renal Failure
The incidence of acute renal failure in patients with HIV-infection is high and the commonest cause is acute tubular necrosis, which usually results from nephrotoxic drugs (pentamidine, aminoglycosides, nonsteroidal anti-inflammatory drugs) or hypotension from dehydration or sepsis. , Hemolytic uremic syndrome (HUS) tends to occur with higher frequency in patients with HIV-infection and has worse prognosis. It can be the presenting illness in patients with HIV-infection. Male homosexuality and intravenous drug abuse are the major risk factors. Similar to idiopathic form, management of HIVassociated HUS includes infusion of fresh frozen plasma, plasma-pheresis and antiplatelet drugs. Although corticosteroids and vincristine can be used, with such a regimen many patients have developed disseminated infections. 
Acute renal failure in patients with HIV infection can also be due to intratubular obstruction, resulting from crystal deposition secondary to drug therapy. The common drugs which lead to crystalluria and renal failure are sulphadiazine, acyclovir (especially if high intravenous dose is used) and protease inhibitors, the most notorious being indinavir. ,,,, Patients usually present with renal colic and renal failure. Typical crystals of actelylsulfadiazine which resemble shocks of wheat; birefringenet needleshaped crystals in case of acyclovir and polyhedric crystals associated with histo cytes with protease inhibitors are usually seen on urinalysis.
Adequate hydration and alkalinization of urine in case of sulphadiazine induced crystalluria lead to rapid resolution of the clinical symptoms. However, some patients with obstruction may require percutaneous nephrostomies and stent placement.
Another interesting cause of renal failure in patients with HIV-infection is granulomatous interstitial infiltration resulting from infiltration of the kidney from disseminated fungal and protozoal infections. Treating the infection can lead to resolution of renal failure in certain cases. ,
Hyponatremia is the commonest electrolyte abnormality seen in patients with HIVinfection and can result from diverse physiologic alterations. ,,, Excessive salt loss from gastrointestinal tract or skin, salt wasting as a result of tubulointerstial renal disease, syndrome of inappropriate antidiuretic hormone (ADH) secretion from opportunistic infections, adrenal insufficiency and administration of hypotonic solutions are some of the causes of hyponatremia in these patients. Hypernatremia is less common, and may also result from dehydration. Diabetes insipidus resulting from foscarnet has been described. 
Hypokalemia may result from excessive vomiting and diarrhea or because of potassium wasting from Amphotericin B therapy.  In contrast, hyperkalemia usually results from hyporeninemic hypo-aldosteronism or adrenal insufficiency.  Elevated potassium levels are also observed in over 75% of patients on high doses of trimethoprime and sulphamethoxazole given for pneumocystis carinii infection. 
Foscarnet, DDI and pentamidine can cause hypocalcemia, and hypomagnesemia often accompanies hypocalcemia. Other causes of hypomagnesemia in HIV-infected patients include magnesium wasting due to amphotericin therapy. Hypercalcemia can occur occasionally as a result of granulomatous diseases, or lymphomas. 
Hypouricemia is observed in over 22% of patients with AIDS and results from high fractional excretion of uric acid in patients with HIV infection for unclear reasons. 
| Conclusion|| |
Patients with HIV-infection can develop a variety of complications such as electrolyte abnormalities, acute and chronic renal failure. These complications could either be a direct consequence of HIV-infection or result from nephrotoxic drugs used for treatment of HIV-infection or associated opportunistic infections. A better awareness of these complications can help clinicians to minimize excessive morbidity related to HIV-infection.
| References|| |
|1.||Rao TK, Filippone EJ, Nicastri AD, et al. Associated focal and segmental glomerulosclerosis in the acquired immunodeficiency syndrome. N Engl J Med 1984; 310:669-73. [PUBMED] |
|2.||Pardo V, Aldana M, Colton RM, et al. Glomerular lesions in the acquired immunodeficiency syndrome. Ann Intern Med 1984;101:429-34. [PUBMED] |
|3.||Glicklich D, Haskell L, Senitzer D, Weiss RA. Possible genetic predisposition to idiopathic focal segmental glomerulosclerosis. Am J Kidney Dis 1988;12:26-30. [PUBMED] |
|4.||Bourgoignie JJ, Ortiz-Interian C, Green DF, Jaffe D, Roth D, Pardo V. The epidemiology of human immunodeficiency virus associated nephropathy. In: Nephrology, edited by Hatano M, Tokyo, SpringerVerlag 1991;484-92. |
|5.||Gardenswartz MH, Lerner CW, Seligson GR, et al. Renal disease in patients with AIDS: a clinicopathologic study. Clin Nephrol 1984;21:197-204. [PUBMED] |
|6.||Pardo V, Meneses R, Ossa L, et al. AIDS-related glomerulopathy: occurrence in specific risk groups. Kidney Int 1987;31:1167-73. [PUBMED] |
|7.||Rao TK, Friedman EA, Nicastri AD. The types of renal disease in the acquired immunodeficiency syndrome. N Engl J Med 1987;316:1062-8. [PUBMED] |
|8.||Valeri A, Neusy AJ. Acute and chronic renal disease in hospitalized AIDS patients. Clin Nephrol 1991;35:110-8. [PUBMED] |
|9.||Frassetto L, Schoenfeld PY, Humphreys MH. Increasing incidence of human immunodeficiency virus-associated nephropathy at San Francisco General Hospital. Am J Kidney Dis 1991;18:655-9. [PUBMED] |
|10.||Winston JA, Klotman PE. Are we missing an epidemic of HIV-associated nephropathy? J Am Soc Nephrol 1996;7:1-7. [PUBMED] |
|11.||Cantor ES, Kimmel PL, Bosch JP. Effect of race on expression of acquired immunodeficiency syndrome-associated nephropathy. Arch Intern Med 1991;151:125-8. [PUBMED] |
|12.||Seney FD Jr, Burns DK, Silva FG. Acquired immunodeficiency syndrome and the kidney. Am J Kidney Dis 1990;16:1-13. |
|13.||Guarda LA, Luna MA, Smith JL Jr, et al. Acquired immune deficiency syndrome. Postmortem findings. Am J Clin Pathol 1984;81:549-57. |
|14.||Hui AN, Koss MN, Meyer PR. Necropsy findings in acquired immuno-deficiency syndrome: a comparison of premortem diagnoses with postmortem findings. Hum Pathol 1984;15:670-6. [PUBMED] |
|15.||Mobley K, Rotterdam HZ, Lerner CW, Tapper ML. Autopsy finding in the acquired immune deficiency syndrome. Pathol Annu 1985;20:45-65. [PUBMED] |
|16.||Niedt GW, Schinella RA. Acquired immunodeficiency syndrome. Clinicopathologic study of 56 autopsies. Arch Pathol Lab Med 1985;109:727-34. |
|17.||Reichert CM, O'Leary TJ, Levens DL, Simrell CR, Macher AM. Autopsy pathology in the acquired immune deficiency syndrome. Am J Pathol 1983;112:357-82. [PUBMED] [FULLTEXT]|
|18.||Mazbar SA, Schoenfeld PY, Humphreys MH. Renal involvement in patients infected with HIV: experience at San Francisco General Hospital. Kidney Int 1990;37:1325-32. [PUBMED] |
|19.||Ahuja TS, Borucki M, Gasic G, Funtanilla M, Hollander M, Rajaraman S. Prevalence of HIV-associated nephropathy in HIV-1 infected patients. JASN 1998;9:82A. |
|20.||Ahuja TS, Agraharkar M, Wilson S. Comparative study of HIV-associated nephropathy and idiopathic collapsing focal segmental sclerosis. JASN 1998;9:82A. |
|21.||Strauss J, Abitbol C, Zilleruelo G, et al. Renal disease in children with the acquired immunodeficiency syndrome. N Engl J Med 1989;321:625-30. [PUBMED] |
|22.||Zilleruelo G, Strauss J. HIV nephropathy in children. Pediatr Clin North Am 1995;42:1469-85. [PUBMED] |
|23.||D'Agati V, Appel GB. HIV infection and the kidney. J Am Soc Nephol 1997;8:138-52. |
|24.||D'Agati V, Suh JI, Carbone L, Cheng JT, Appel G. Pathology of HIV-associated nephropathy: a detailed morphologic and comparative study. Kidney Int 1989;35: 1358-70. [PUBMED] |
|25.||Green DF, Resnick L, Bourgoignie JJ. HIV infects glomerular endothelial and mesangial but not epithelial cells in vitro. Kidney Int 1992;41:956-60. [PUBMED] |
|26.||Alpers CE, McClure J, Bursten SL. Human mesangial cells are resistant to productive infection by multiple strains of human immunodeficiency virus types 1 and 2. Am J Kidney Dis 1992;19:126-30. [PUBMED] |
|27.||Kimmel PL, Ferreira-Centeno A, FarkasSzallasi T, Abraham AA, Garrett CT. Viral DNA in microdissected renal biopsy tissue from HIV infected patients with nephrotic syndrome. Kidney Int 1993;43: 1347-52. [PUBMED] |
|28.||Dickie P, Felser J, Eckhaus M, et al. HIV associated nephropathy in transgenic mice expressing HIV-1 genes. Virology 1991; 185:109-19. [PUBMED] [FULLTEXT]|
|29.||Kopp JB, Klotman ME, Adler SH, et al. Progressive glomerulosclerosis and enhanced renal accumulation of basement membrane components in mice transgenic for human immunodeficiency virus type 1 genes. Proc Natl Acad Sci USA 1992;89:1577-81. [PUBMED] [FULLTEXT]|
|30.||Kopp JB, Ray PE, Adler SH, et al. Nephropathy in HIV-transgenic mice. Contrib Nephrol 1994;107:194-204. [PUBMED] |
|31.||Ray PE, Bruggeman LA, Weeks BS, et al. bFGF and its low affinity receptors in the pathogenesis of HIV-associated nephropathy in transgenic mice. Kidney Int 1994;46:759-72. [PUBMED] |
|32.||Winston J, Klotman PE, Klotman M. Plasma HIV-1 RNA in Seropositive patients with renal disease. JASN 1996;7:1345. |
|33.||Mattana J, Siegal FP, Schwarzwald E, et al. AIDS-associated membranous nephropathy with advanced renal failure: response to prednisone. Am J Kidney Dis 1997;30:116-9. [PUBMED] |
|34.||Detwiler RK, Falk RJ, Hogan SL, Jennette JC. Collapsing glomerulopathy: a clinically and pathologically distinct variant of focal segmental glomerulosclerosis. Kidney Int 1994;45:1416-24. [PUBMED] |
|35.||Ifudu O, Rao TK, Tan CC, Fleischman H, Chirgwin K, Friedman EA. Zidovudine is beneficial in Human immunodeficiency virus associated nephropathy. Am J Nephrol 1995;15:217-21. [PUBMED] |
|36.||Kimmel PL, Mishkin GJ, Umana WO. Captopril and renal survival in patients with human immunodeficiency virus nephropathy. Am J Kidney Dis 1996;28: 202-8. [PUBMED] |
|37.||Burns GC, Paul SK, Toth IR, Sibak SL. Effect of angiotensin-converting enzyme inhibition in HIV-associated nephropathy. J Am Soc Nephrol 1997;8:1140-6. |
|38.||Smith MC, Pawar R, Carey JT, et al. Effect of corticosteroid therapy on human immunodeficiency virus associated nephropathy. Am J Med 1994;97:145-51. [PUBMED] [FULLTEXT]|
|39.||Smith MC, Austen JL, Carey JT, et al. Prednisone improves renal function and proteinuria in human immunodeficiency virus-associated nephropathy. Am J Med 1996;101:41-8. [PUBMED] [FULLTEXT]|
|40.||Ingulli E, Tejani A, Fikrig S, et al. Nephrotic syndrome associated with acquired immunodeficiency syndrome in children. J Pediatr 1991;119:710-6. [PUBMED] |
|41.||Ifudu O, Mayers JD, Matthew JJ, et al. Uremia therapy in patients with end-stage renal disease and human immunodeficiency virus infection: Has the outcome changed in the 1990s?Am J Kidney Dis 1997;29:549-52. [PUBMED] |
|42.||Ahuja TS, Niaz N, Velasco A, Watts B 3rd, Paar D. Effect of hemodialysis and antiretroviral therapy on plasma viral load in HIV-1 infected hemodialysis patients. Clin Nephrol 1999;51:40-4. [PUBMED] |
|43.||Tzakis AG, Cooper MH, Dummer JS, Ragni M, Ward JW, Starzl TE. Transplantation in HIV+ patients. Transplantation 1990;49:354-8. [PUBMED] |
|44.||Ahuja TS, Zingman B, Glicklich D. Longterm survival in an HIV-infected renal transplants recipient. Am J Nephrol 1997;17: 480-2. [PUBMED] |
|45.||Rao TK. Acute renal failure syndromes in human immunodeficiency virus infection. Semin Nephrol 1998;18:378-95. [PUBMED] |
|46.||Rao TK, Friedman EA. Outcome of severe acute renal failure in patients with acquired immunodeficiency syndrome. Am J Kidney Dis 1995;25:390-8. [PUBMED] |
|47.||Berns JS, Hemolytic-uremic syndrome and thormbotic thombocytopenic purpura associated with HIV infection, in Kimmel PL, Bern JS (eds): Renal and urologic aspects of HIV-infection. New York, NY, Churchill Livingstone 1995;111-33. |
|48.||Becker K, Jablonowski H, Haussinger D. Sulfadiazine-associated nephrotoxicity in patients with acquired immunodeficiency syndrome. Medicine Baltimore 1996;75: 185-94. |
|49.||Eck P, Silver SM, Clark EC. Acute renal failure and coma after a high dose of oral acyclovir. N Engl J Med 1991;325:1178-9. [PUBMED] |
|50.||Peterslund NA, Black FT, Tauris P. Impaired renal function after bolus injection of acyclovir. Lancet 1983;1:243-4. [PUBMED] |
|51.||Kopp JB, Miller KD, Mican JM, et al. Crystalluria and urinary tract abnor-malities associated with indinavir. Ann Intern Med 1997;127:119-25. |
|52.||Tashima KT, Horowitz JD, Rosen S. Indinavir nephropathy. N Engl J Med 1997;336:138-40. [PUBMED] |
|53.||Ahuja TS, Remmers A, Rajaraman S, Funtanilla M. Acute renal failure in a patient with AIDS: histoplasmosis-induced granulomatous interstitial nephritis. Am J Kidney Dis 1998;32:E3. |
|54.||Aarons EJ, Woodrow D, Hollister WS, et al. Reversible renal failure caused by a microsporidian infection. AIDS 1994;8:1119-21. [PUBMED] |
|55.||Anderson RJ. Hospital associated hyponatremia. Kidney Int 1986;29:1237-47. [PUBMED] |
|56.||Tang WW, Kaptein EM, Feinstein EI, Massry SG. Hyponatremia in hospitalized patients with the acquired immunodeficiency syndrome (AIDS) and AIDS-related complex. Am J Med 1993;94:169-74. [PUBMED] [FULLTEXT]|
|57.||Peter SA. Electrolyte disorders and renal dysfunction in acquired immunodeficiency syndrome patients. J Natl Med Assoc 1991;83:889-91. [PUBMED] |
|58.||Farese RV Jr, Schambelan M, Hollander H, Stringari S, Jacobson MA. Nephro-genic diabetes insipidus associated with foscarnet treatment of cytomegalovirus retinitis. Ann Intern Med 1990;112:955-6. [PUBMED] |
|59.||Marks JB. Endocrine manifestations of human immunodeficiency virus (HIV) infection. Am J Med Sci 1991;302:110-7. [PUBMED] |
|60.||Greenberg S, Reiser IW, Chou SY. Hyperkalemia with high-dose trimethoprimsulphamethaxazole therapy. Am J Kidney Dis 1993;22:603-6. [PUBMED] |
|61.||Peter SA. Disorders of serum calcium in acquired immunodeficiency syndrome. J Natl Med Assoc 1992;84:626-8. [PUBMED] |
|62.||Maesaka JK, Cusano AJ, Thies HL, Siegal FP, Dreisbach. Hypouricemia in acquired immuno-deficiency syndrome. Am J Kidney Dis 1990;15:252-7. |
Tejinder S Ahuja
Division of Nephrology, The University of Texas Medical Branch, 4,200 John Sealy Annex, 301 University Boulevard, Galveston, Texas 77555-0562
[Figure - 1], [Figure - 2], [Figure - 3]
[Table - 1]
| Article Access Statistics|
| Viewed||3111 |
| Printed||63 |
| Emailed||0 |
| PDF Downloaded||387 |
| Comments ||[Add] |