eMedicine Specialties > Nephrology > The Kidney in Systemic Diseases
HIV Nephropathy
Updated: Feb 4, 2009
Introduction
Human immunodeficiency virus (HIV) infection can cause a broad spectrum of clinical manifestations, ranging from an asymptomatic carrier state to severe immunodeficiency. Renal disease is a relatively common complication in patients with HIV disease.1 Renal disease can result from direct kidney infection with HIV or from the adverse effects of medications used to treat the virus.2,3 Further, patients with HIV disease are at risk for developing prerenal azotemia due to volume depletion resulting from salt wasting, poor nutrition, nausea, or vomiting.
HIV-associated nephropathy (HIVAN), formerly known as AIDS-associated nephropathy, is characterized by the following findings:
- Nephrotic range proteinuria
- Azotemia
- Normal to large kidneys on ultrasonographic images
- Normal pressure
- Focal segmental glomerulosclerosis (FSGS) on renal biopsy findings
Once HIVAN was diagnosed, rapid progression to renal failure and end-stage renal disease (ESRD), leading to the need for dialysis, was the norm in the preantiretroviral therapy era. Highly active antiretroviral therapy (HAART) has changed the natural course of this disease. Although FSGS is the predominant glomerular lesion in HIVAN, other reported glomerular lesions in patients with HIV include IgA nephropathy, cryoglobulinemia, amyloidosis, and a lupuslike immune complex glomerulopathy. Physicians must consider HIVAN in patients who are seropositive for HIV and have proteinuria.
For excellent patient education resources, visit eMedicine's Immune System Center and Sexually Transmitted Diseases Center. Also, see eMedicine's patient education articles HIV/AIDS and Rapid Oral HIV Test.
Related eMedicine topics:
Acute Renal Failure
Azotemia
Chronic Renal Failure
Focal Segmental Glomerulosclerosis
HIV Infection
HIV Infection and AIDS
HIV Infection, Antiretroviral Therapy
Renal Failure, Acute
Epidemiology
According to the US Renal Data System (USRDS), HIV-associated nephropathy (HIVAN) accounts for approximately 1% of new ESRD cases in the United States. HIVAN is observed in patients regardless of the route by which HIV was contracted. HIVAN is observed predominantly among African Americans and is the third leading cause of ESRD among black persons aged 20-64 years.4,5 Most patients with HIVAN are young black males, and approximately 50% are intravenous addicts.6 Overall, HIVAN is observed more often in men than in women, with a male to female ratio of 10:1. The mean age of persons with HIVAN is 33 years.
Pathogenesis
Experiments using transgenic mice have provided perhaps the strongest evidence for a direct role by HIV type 1 (HIV-1) in the development of HIV-associated nephropathy (HIVAN). Researchers created transgenic mice by inserting HIV deoxyribonucleic acid (DNA) constructs into the mice's genomes. The mice developed proteinuria and had a histologic picture similar to that observed in patients with HIVAN. A genetic or environmental cofactor that has not yet been identified is required for patients to develop this disease, which may explain the racial predilection for HIVAN among black persons.4
The cellular target in the development of HIVAN is probably the renal glomerular and tubular epithelium. Using in situ hybridization and polymerase chain reaction assays to detect HIV-1 DNA and messenger ribonucleic acid (mRNA), investigators have shown that renal glomerular and tubular epithelial cells are productively infected by HIV-1 in patients with HIVAN; this argues strongly for localized replication of HIV-1 in the kidney and for the existence of a renal viral reservoir. Further, circularized viral DNA, a marker of recent nuclear import of full-length, reverse-transcribed RNA, has been detected in kidney biopsy samples from patients with HIVAN, suggesting active replication in renal tissue. However, the mechanisms of virus-induced renal injury remain undetermined.
Peculiar histopathologic features of HIVAN are the enhanced proliferation and the loss of differentiation markers of glomerular epithelial cells. In one study, HIV-1 infection was shown to kill renal tubular epithelial cells in vitro by triggering an apoptotic pathway involving caspase activation and Fas up-regulation, suggesting that apoptosis of nonlymphoid cells can be directly induced by HIV-1. The net and long-standing glomerular and tubular epithelial cell damage leads to proteinuria, glomerulosclerosis, and tubulointerstitial scarring.
The role of cytokines has not been established, and although their presence is not essential for the development of HIVAN, cytokines may modify the progression of infection or a patient's susceptibility to infection. The levels of cytokines are increased in renal biopsy samples from patients with HIVAN. In one study, mesangial and tubular cell production of interleukin-6 and tumor necrosis factor – alpha was shown to be a potent stimulus for HIV-1 expression in HIV-1 – infected monocytes.7 Viral replication in response to cytokines may play an important role in the pathogenesis of HIVAN.
Genetics
The reason behind the increased predilection among black persons for the development of HIV-associated nephropathy is not clear.4 In general, black persons have a higher incidence of other renal diseases (eg, diabetic nephropathy, lupus, abuse); therefore, they may have an underlying genetic predisposition to severe renal disease, regardless of the etiology. The type of host response to the HIV infection itself may be what determines whether or not nephropathy develops in a specific individual.
Histology
When examined using ultrasonography or computed tomography (CT) scanning, patients with HIV-associated nephropathy (HIVAN) have enlarged and echogenic kidneys. This may result from prominent interstitial expansion by cellular infiltrate and markedly dilated tubules containing voluminous casts.
Findings from light microscopy of kidney biopsy tissue are diagnostic in most cases. The most common histologic light microscopy finding is a collapsing form of focal segmental glomerulosclerosis.8 The glomerular capillary tuft is collapsed (see first image below and Image 1) and may be segmentally or globally sclerosed. Visceral epithelial cells are hypertrophied and form a characteristic pseudocrescent in the Bowman space. Tubulointerstitial scarring, atrophy, and marked dilatation of the tubules (microcystic dilatations) are usually present (see second image below and Image 2).
Immunofluorescent microscopy helps to identify positive staining for albumin and immunoglobulin G in epithelial cells and for immunoglobulin M, C3, and (occasionally) A in mesangial or sclerotic areas. Electron microscopy reveals wrinkling of the basement membranes, epithelial cell proliferation, and focal foot process effacement. Tubuloreticular structures in the glomerular endothelial cells (see third image below and Image 3), consisting of ribonucleoprotein and membrane, the synthesis of which is stimulated by alpha interferon, is highly predictive of HIVAN.
Light microscopy with trichrome staining showing the collapse of the glomerular tuft, with segmental glomerular and interstitial sclerosis (bluish staining). The renal tubules are dilated and filled with proteinaceous material.
Light microscopy showing prominent microcystic dilatation of renal tubules filled with proteinaceous material; this finding is characteristic of human immunodeficiency virus (HIV)–associated nephropathy, although it may also be observed in chronic glomerulonephritis.
Electron microscopy showing a segment of the glomerular basement membrane; foot process effacement (black arrow) and prominent tubuloreticular inclusions (red arrow) are present.
Clinical Features
Patients with HIV-associated nephropathy (HIVAN) typically present with a nephrotic syndrome consisting of nephrotic-range proteinuria (>3.5 g/d), azotemia, hypoalbuminemia, and hyperlipidemia. Edema is uncommon in HIVAN, yet many authors think that this is a characteristic of HIVAN. The salt-losing propensity and high oncotic pressure contributed by marked hypergammaglobulinemia in these patients have been suggested as possible explanations for this puzzling observation. The CD4 count in patients with HIVAN is usually depressed below 200 cells/µL, but HIVAN has been reported in patients with higher CD4 counts. The prognosis for renal survival is worse in patients with clinical acquired immunodeficiency syndrome (AIDS), especially if their CD4 count is less than 50 cells/µL.
Patients with HIVAN are not typically hypertensive, even in the face of renal insufficiency, and their kidneys are usually normal to large in size and highly echogenic on ultrasonograms. Routine urinalysis may occasionally reveal findings of nonnephrotic proteinuria in patients being evaluated for other medical conditions. The urinalysis reveals microhematuria, leukocytes, hyaline casts, and oval fat bodies, but no cellular casts. Serum complement levels are normal.
In one study, the rate of progression from the initial presentation to ESRD was 2.5 months in the pre-HAART era. With the introduction of HAART in 1996-1997, the traditional natural history of rapid progression of HIVAN has been slowed significantly. HAART therapy has been shown to retard the progression of renal disease in persons with HIVAN.
Electrolyte abnormalities, such as hyponatremia and hyperkalemia, may be observed in patients with HIVAN and may reflect an increase in total body water (from nephrotic syndrome or syndrome of inappropriate secretion of antidiuretic hormone [SIADH]) or from hyporeninemic hypoaldosteronism, respectively. SIADH may result from concomitant pulmonary infection or from persistent nausea from medications or gastrointestinal disease. Hyporeninemic hypoaldosteronism, a cause of type IV renal tubular acidosis manifesting as hyperkalemia with normal anion gap metabolic acidosis, is much more common when renal insufficiency is present.
Most HIV medications are well tolerated, even in the presence of renal insufficiency. The (potential) toxicity of the nucleoside reverse transcriptase inhibitors (ie, zidovudine,9 didanosine, zalcitabine, stavudine, lamivudine, abacavir, emtricitabine) uniformly manifests as type-B lactic acidosis. However, didanosine may cause electrolyte abnormalities, such as hypokalemia, hyponatremia, hypermagnesemia, and hyperuricemia, and stavudine may cause hyperuricemia. Tenofovir is a nucleotide reverse transcriptase inhibitor with known renal toxicity and hypophosphatemia and therefore dose adjustment is indicated when creatinine clearance is less than 50 mL/min. Except for nevirapine, which may cause lactic acidosis, the nonnucleoside reverse transcriptase inhibitors (ie, nevirapine, delavirdine, efavirenz, etravirine) have no reported significant renal toxicity.
As a class, the protease inhibitors (ie, saquinavir, ritonavir, indinavir, nelfinavir, amprenavir, fosamprenavir, lopinavir, atazanavir, tipranavir, darunavir) may precipitate nephrolithiasis. A classic form of this is indinavir crystalluria, which occurs independently of renal function; however, the stones resolve after cessation of indinavir therapy. Enfuvirtide (Fuzeon) is the first of a newer class of fusion inhibitors that targets the gp41 protein on HIV's surface and stops the virus from entering cells. Enfuvirtide has no known renal effects for creatinine clearance of greater than 35 mL/min.
Maraviroc (Selzentry), approved in August 2007, is also a fusion inhibitor that targets the CCR5 protein and stops the virus from entering cells. Selzentry does not require dose adjustment for creatinine clearance greater than 50 mL/min. Raltegravir (Isentress) is the first of a newer class of integrase strand transfer inhibitors; it does not require dose adjustment inpatients with abnormal renal function.
Dose adjustment should be made in patients receiving nucleoside reverse transcriptase inhibitors when the glomerular filtration rate falls below 50 mL/min. Patients receiving nonnucleoside reverse transcriptase inhibitors may also receive a dose adjustment when the glomerular filtration rate falls below 50 mL/min. No dose adjustment is required for patients taking protease inhibitors. Some drugs used to treat opportunistic infections in HIV disease may also cause nephrotoxicity or electrolyte abnormalities (see image below and Image 4).
Types of electrolyte abnormalities observed with some of the drugs used to treat opportunistic infections in patients with human immunodeficiency virus (HIV). ARF stands for acute renal failure.
Indications for Biopsy
The decision to obtain a biopsy sample is somewhat controversial in the general medical community. Even if a patient presents with the classic clinical features of HIV-associated neuropathy (HIVAN), clinical consideration is predictive of the biopsy diagnosis in only 55-60% of patients. Therefore, to distinguish HIVAN from other forms of renal disease (eg, immune complex glomerulonephritis, immunoglobulin-A nephropathy), patients who are seropositive for HIV require a renal biopsy. The typical practice is to obtain a renal biopsy specimen if the patient's daily protein excretion is greater than 1 gram.
Treatment
Antiretroviral therapy
The best course of treatment involves a collaborative effort between a nephrologist and an HIV disease specialist.3 The current United States Public Health Service standard is to initiate aggressive combination antiretroviral therapy (ie, HAART) for all patients with advanced or symptomatic HIV disease, or advanced disease defined as a CD4 count of fewer than 350 cells/µL. Other authorities and guidelines also recommend therapy for an HIV plasma viral load of greater than 100,000/ml. Although there are no guiding clinical studies, some experts recommend consideration of therapy in all patients with HIV-associated nephritis (HIVAN). A report from the USRDS shows that the incidence of HIVAN appears to have declined since the introduction of HAART.
HAART is in constant evolution. The reader is referred to other chapters in this text for specific information, including recommendations for dosage adjustments for renal insufficiency.
Angiotensin-converting enzyme (ACE) inhibitors
In patients with advanced renal insufficiency, captopril was noted to improve renal survival for a mean length of 37-156 days.10 In a subsequent prospective follow-up of 44 patients, the median length of renal survival for patients who received fosinopril was 479.5 days, with only 1 patient developing ESRD. All untreated control subjects progressed to ESRD, with a median length of renal survival of 146.5 days (P <0.0001). The exact mechanism of action of this class of drugs is unknown, but it may be related to a hemodynamic effect, a reduction in the transglomerular passage of serum proteins, and an antiproliferative effect mediated in part by the inhibition of transforming growth factor beta. Use ACE inhibitors if patients do not have hyperkalemia.
CorticosteroidsA number of case reports have suggested that corticosteroids offer some short-term benefit.11 In one report, results from a pretreatment and posttreatment kidney biopsy suggested that an improvement in renal function was associated with a reduced number of lymphocytes and macrophages infiltrating the interstitium. In another report, 20 patients were treated with prednisone at 60 mg/d for 2-11 weeks, followed by a slow taper.12 After a follow-up of 44 weeks, 8 patients required maintenance dialysis, 11 died from complications, and 7 were alive and no longer had ESRD.
Cyclosporine
Some reports on pediatric populations suggest that cyclosporine can be effective in reducing the proteinuria observed in persons with HIVAN. The usefulness of cyclosporine therapy for HIVAN warrants further study.
Promising therapeutic strategies in animal studies
Animal research shows promising results for retarding renal disease progression in HIVAN. In one study, the use of a cyclin-dependent kinase inhibitor decreased visceral epithelial cell proliferation in HIV-infected mice.13 In another study, blocking nuclear factor kappa beta (a cell signaling pathway) in mice resulted in increased lifespan and kidney and lean body mass preservation.14 These benefits were associated with a reduction in the number of CD45(+) cells infiltrating the kidneys, amelioration of the renal architecture, and a reduction in the level of circulating inflammatory cytokines. Further studies are needed to determine the role of these inhibitors on human HIVAN.
Dialysis and transplantation
Patients with HIVAN who progress to ESRD remain a clinical challenge. Physicians must anticipate progressive renal disease in patients with HIVAN and have as a goal the placement of an arteriovenous fistula in a timely manner for future use in hemodialysis. In current practice, hemodialysis is the accepted modality of ESRD therapy in these patients. Because of increased susceptibility to infections, peritoneal dialysis has not been widely advocated.
For the same reason, the general theory is that immunosuppression after kidney transplantation would pose a substantive risk of opportunistic infections in patients with HIVAN.15 Consequently, kidney transplantation in these patients is still considered experimental, with only a few transplant centers considering cadaver kidney transplantation in compliant, stable patients with no prior opportunistic infections who have an undetectable viral load and a CD4 count of more than 300 cells/µL. Anecdotal reports drawn from small samples of this selected group of patients with HIVAN suggest no extra risk of opportunistic infections; however, until larger studies are performed, transplantation in persons with HIVAN remains relatively contraindicated.
In one study, 1- and 2-year actuarial patient survival was 85% and 82%, respectively, and graft survival was 75% and 71%, respectively. Plasma HIV-1 RNA remained undetectable, and CD4 counts remained in excess of 400 cells/µL with no evidence of AIDS for up to 2 years. These results were comparable to other high-risk populations receiving kidney transplantation.
Related eMedicine topics:
Kidney Transplantation
Kidney Transplantation, Surgical Complications
Renal Failure, Chronic and Dialysis Complications
Renal Transplantation (Medical)
Transplants, Renal
Multimedia
 | Media file 1:
Light microscopy with trichrome staining showing
the collapse of the glomerular tuft, with segmental glomerular
and interstitial sclerosis (bluish staining). The renal tubules
are dilated and filled with proteinaceous
material. |
 | Media file 2:
Light microscopy showing prominent microcystic
dilatation of renal tubules filled with proteinaceous material;
this finding is characteristic of human
immunodeficiency virus (HIV)–associated nephropathy,
although it may also be observed in chronic
glomerulonephritis. |
 | Media file 3: Electron microscopy showing a segment of the glomerular basement membrane; foot process effacement (black arrow) and prominent tubuloreticular inclusions (red arrow) are present. |
 | Media file 4: Types of electrolyte abnormalities observed with some of the drugs used to treat opportunistic infections in patients with human immunodeficiency virus (HIV). ARF stands for acute renal failure. |
Keywords
HIV nephropathy, AIDS, HIV, kidney, kidneys, kidney disease, failure renal, kidney failure, renal disease, kidney problems, ESRD, end stage renal failure, end stage renal disease, nephropathy, antiretroviral, antiretroviral therapy, end stage kidney disease, acquired immune deficiency syndrome, acquired immunodeficiency syndrome, HIV associated nephropathy, HIV-associated nephropathy, HIVAN, HIV-related nephropathy, HIV infection, HIV disease, AIDS-related nephropathy, AIDS associated nephropathy, AIDS-associated nephropathy, renal disease, end-stage renal disease,kidney infection, pre-renal azotemia, prerenal azotemia, focal segmental glomerulosclerosis, FSGS, renal failure, anti-retroviral therapy, proteinuria, virus-induced renal injury, viral-induced renal injury, virus-induced kidney injury, viral-induced kidney injury
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References
Wyatt CM, Morgello S, Katz-Malamed R, et al. The spectrum of kidney disease in patients with AIDS in the era of antiretroviral therapy. Kidney Int. Feb 2009;75(4):428-34. [Medline].
Kalim S, Szczech LA, Wyatt CM. Acute kidney injury in HIV-infected patients. Semin Nephrol. Nov 2008;28(6):556-62. [Medline].
Atta MG, Deray G, Lucas GM. Antiretroviral nephrotoxicities. Semin Nephrol. Nov 2008;28(6):563-75. [Medline].
Schwartz EJ, Klotman PE. Pathogenesis of human immunodeficiency virus (HIV)-associated nephropathy. Semin Nephrol. Jul 1998;18(4):436-45. [Medline].
Winston JA, Burns GC, Klotman PE. Treatment of HIV-associated nephropathy. Semin Nephrol. May 2000;20(3):293-8. [Medline].
Carbone L, D'Agati V, Cheng JT, et al. Course and prognosis of human immunodeficiency virus-associated nephropathy. Am J Med. Oct 1989;87(4):389-95. [Medline].
O''Donnell MP, Chao CC, Gekker G, et al. Renal cell cytokine production stimulates HIV-1 expression in chronically HIV-1-infected monocytes. Kidney Int. Mar 1998;53(3):593-7. [Medline]. [Full Text].
Chan KT, Papeta N, Martino J, et al. Accelerated development of collapsing glomerulopathy in mice congenic for the HIVAN1 locus. Kidney Int. Feb 2009;75(4):366-72. [Medline].
Ifudu O, Rao TK, Tan CC, et al. Zidovudine is beneficial in human immunodeficiency virus associated nephropathy. Am J Nephrol. 1995;15(3):217-21. [Medline].
Kimmel PL, Mishkin GJ, Umana WO. Captopril and renal survival in patients with human immunodeficiency virus nephropathy. Am J Kidney Dis. Aug 1996;28(2):202-8. [Medline].
Eustace JA, Nuermberger E, Choi M, et al. Cohort study of the treatment of severe HIV-associated nephropathy with corticosteroids. Kidney Int. Sep 2000;58(3):1253-60. [Medline]. [Full Text].
Smith MC, Austen JL, Carey JT, et al. Prednisone improves renal function and proteinuria in human immunodeficiency virus-associated nephropathy. Am J Med. Jul 1996;101(1):41-8. [Medline].
Gherardi D, D'Agati V, Chu TH, et al. Reversal of collapsing glomerulopathy in mice with the cyclin-dependent kinase inhibitor CYC202. J Am Soc Nephrol. May 2004;15(5):1212-22. [Medline]. [Full Text].
Heckmann A, Waltzinger C, Jolicoeur P, et al. IKK2 inhibitor alleviates kidney and wasting diseases in a murine model of human AIDS. Am J Pathol. Apr 2004;164(4):1253-62. [Medline]. [Full Text].
Sawinski D, Murphy B. End-stage renal disease and kidney transplant in HIV-infected patients. Semin Nephrol. Nov 2008;28(6):581-4. [Medline].
Abbott KC, Hypolite I, Welch PG, et al. Human immunodeficiency virus/acquired immunodeficiency syndrome-associated nephropathy at end-stage renal disease in the United States: patient characteristics and survival in the pre-highly active antiretroviral therapy era. J Nephrol. Sep-Oct 2001;14(5):377-83. [Medline].
Berggren R, Batuman V. HIV-associated renal disorders: recent insights into pathogenesis and treatment. Curr HIV/AIDS Rep. Aug 2005;2(3):109-15. [Medline].
Bruggeman LA, Ross MD, Tanji N, et al. Renal epithelium is a previously unrecognized site of HIV-1 infection. J Am Soc Nephrol. Nov 2000;11(11):2079-87. [Medline]. [Full Text].
Choi AI, Rodriguez RA. Renal manifestations of HIV. HIV InSite. Available at http://hivinsite.ucsf.edu/InSite.jsp?page=kb-04-01-10. Accessed 2/3/09.
Conaldi PG, Bottelli A, Baj A, et al. Human immunodeficiency virus-1 tat induces hyperproliferation and dysregulation of renal glomerular epithelial cells. Am J Pathol. Jul 2002;161(1):53-61. [Medline]. [Full Text].
Dave MB, Shabih K, Blum S. Maintenance hemodialysis in patients with HIV-associated nephropathy. Clin Nephrol. Dec 1998;50(6):367-74. [Medline].
Dominguez S, Ghosn J, Peytavin G, et al. Efficacy and safety of tenofovir double-dose in treatment-experienced HIV-infected patients: the TENOPLUS study. J Med Virol. Feb 2007;79(2):105-10. [Medline].
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. Apr 1997;29(4):549-52. [Medline].
Kiryluk K, Martino J, Gharavi AG. Genetic susceptibility, HIV infection, and the kidney. Clin J Am Soc Nephrol. Jul 2007;2 Suppl 1:S25-35. [Medline]. [Full Text].
Klotman PE. HIV-associated nephropathy. Kidney Int. Sep 1999;56(3):1161-76. [Medline]. [Full Text].
Marras D, Bruggeman LA, Gao F, et al. Replication and compartmentalization of HIV-1 in kidney epithelium of patients with HIV-associated nephropathy. Nat Med. May 2002;8(5):522-6. [Medline].
Rao TK. Human immunodeficiency virus (HIV) associated nephropathy. Annu Rev Med. 1991;42:391-401. [Medline].
Rao TK. Human immunodeficiency virus infection and renal failure. Infect Dis Clin North Am. Sep 2001;15(3):833-50. [Medline].
Ray PE, Xu L, Rakusan T, et al. A 20-year history of childhood HIV-associated nephropathy. Pediatr Nephrol. Oct 2004;19(10):1075-92. [Medline].
Rose BD, Appel GB. Collapsing FGS and renal disease associated with HIV infection. Up-To-Date [serial online]. 8:2.
Schwartz EJ, Szczech LA, Ross MJ, et al. Highly active antiretroviral therapy and the epidemic of HIV+ end-stage renal disease. J Am Soc Nephrol. Aug 2005;16(8):2412-20. [Medline]. [Full Text].
Szczech LA, Gupta SK, Habash R, et al. The clinical epidemiology and course of the spectrum of renal diseases associated with HIV infection. Kidney Int. Sep 2004;66(3):1145-52. [Medline].
Wei A, Burns GC, Williams BA. Long-term renal survival in HIV-associated nephropathy with angiotensin-converting enzyme inhibition. Kidney Int. Oct 2003;64(4):1462-71. [Medline].
Winston J, Klotman PE. HIV-associated nephropathy. Mt Sinai J Med. Jan 1998;65(1):27-32. [Medline].
Winston JA, Klotman ME, Klotman PE. HIV-associated nephropathy is a late, not early, manifestation of HIV-1 infection. Kidney Int. Mar 1999;55(3):1036-40. [Medline]. [Full Text].
Wyatt CM, Klotman PE. HIV-1 and HIV-associated nephropathy 25 years later. Clin J Am Soc Nephrol. Jul 2007;2 Suppl 1:S20-4. [Medline]. [Full Text].
Further Reading
Keywords
HIV nephropathy, AIDS, HIV, kidney, kidneys, kidney disease, failure renal, kidney failure, renal disease, kidney problems, ESRD, end stage renal failure, end stage renal disease, nephropathy, antiretroviral, antiretroviral therapy, end stage kidney disease, acquired immune deficiency syndrome, acquired immunodeficiency syndrome, HIV associated nephropathy, HIV-associated nephropathy, HIVAN, HIV-related nephropathy, HIV infection, HIV disease, AIDS-related nephropathy, AIDS associated nephropathy, AIDS-associated nephropathy, renal disease, end-stage renal disease,kidney infection, pre-renal azotemia, prerenal azotemia, focal segmental glomerulosclerosis, FSGS, renal failure, anti-retroviral therapy, proteinuria, virus-induced renal injury, viral-induced renal injury, virus-induced kidney injury, viral-induced kidney injury
