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Collapsing glomerulopathy is a pattern of renal injury that has emerged along with the epidemic of HIV infection. The disease process is now increasingly recognized in non-HIV patients. In HIV and non-HIV patients the disease shares many clinical and pathologic features, and, we presume, pathogenetic factors. The disease entity is characterized by very heavy proteinuria frequently combined with rapidly progressive renal failure, poor outcome, glomerular collapse with hyperplasia and other degenerative changes of the visceral epithelial cells, and prominent tubulointerstitial injury with frequent microcystic changes. HIV-associated nephropathy has a higher prevalence in blacks, high frequency of intra-endothelial tubuloreticular inclusions, and prominent microcystic tubular changes. These differences, however, are not sufficient to predict the patient's HIV status from the biopsy findings alone. Collapsing glomerulopathy can also develop in association with lymphoproliferative disorders, systemic lupus erythematosus-like and other autoimmune diseases, other immune deficiency syndromes and viral infections, and in the context of immunosuppressive therapy.
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PMID:Collapsing glomerulopathy--a new pattern of renal injury. 1218 Jun 32

Collapsing glomerulopathy is a pathologic diagnosis characterized by obliteration of glomerular capillary lumina, seen most commonly as a primary glomerular disease in young black men. A secondary form with almost identical pathologic features is described in association with human immunodeficiency virus infection. The disease is characterized by heavy proteinuria with variable renal insufficiency at the onset followed by rapid progression to end-stage renal disease with no documented effective therapy. We describe a patient who presented with systemic manifestations, including fever, acute renal failure with massive proteinuria, and noncardiogenic pulmonary edema. Renal biopsy showed classic collapsing glomerulopathy. All known causes of noncardiogenic pulmonary edema were ruled out. The pulmonary syndrome resolved, but the renal disease progressed to end-stage renal disease. We propose consideration of collapsing glomerulopathy in the differential diagnosis of any patient presenting with a multisystem disease including acute renal failure and pulmonary edema.
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PMID:Collapsing glomerulopathy: a cause of noncardiogenic pulmonary edema. 1220 Aug 27

Kidney disease affects over 20 million people in the United States alone. Although the causes of renal failure are diverse, the glomerular filtration barrier is often the target of injury. Dysregulation of VEGF expression within the glomerulus has been demonstrated in a wide range of primary and acquired renal diseases, although the significance of these changes is unknown. In the glomerulus, VEGF-A is highly expressed in podocytes that make up a major portion of the barrier between the blood and urinary spaces. In this paper, we show that glomerular-selective deletion or overexpression of VEGF-A leads to glomerular disease in mice. Podocyte-specific heterozygosity for VEGF-A resulted in renal disease by 2.5 weeks of age, characterized by proteinuria and endotheliosis, the renal lesion seen in preeclampsia. Homozygous deletion of VEGF-A in glomeruli resulted in perinatal lethality. Mutant kidneys failed to develop a filtration barrier due to defects in endothelial cell migration, differentiation, and survival. In contrast, podocyte-specific overexpression of the VEGF-164 isoform led to a striking collapsing glomerulopathy, the lesion seen in HIV-associated nephropathy. Our data demonstrate that tight regulation of VEGF-A signaling is critical for establishment and maintenance of the glomerular filtration barrier and strongly supports a pivotal role for VEGF-A in renal disease.
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PMID:Glomerular-specific alterations of VEGF-A expression lead to distinct congenital and acquired renal diseases. 1261 13

HIV-associated nephropathy is a unique form of renal disease specific to HIV infection. Proteinuria and rapidly worsening azotemia in the absence of edema and hypertension are characteristic. Renal biopsy reveals collapsing and/or sclerotic glomeruli, microcystic tubular dilatation, and cellular interstitial infiltrates. Direct cytopathic effects of HIV in the setting of a particular cytokine milieu appears to be the mechanism responsible for the renal injury. There is limited therapeutic experience, but trials with steroids and angiotensin-converting enzyme inhibitors are encouraging. Dialysis is the main form of renal replacement therapy. Better understanding of the disease should improve treatment and prognosis.
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PMID:HIV-associated nephropathy: clinical characteristics and therapeutic options. 1272 79

The most common manifestation of HIV/AIDS in the kidney is the collapsing variant of focal segmental glomerular sclerosis, HIV-associated nephropathy (HIVAN). Other forms of renal disease in HIV-infected patients include mesangial proliferative glomerulonephritis (GN), membranoproliferative GN, IgA nephropathy, minimal change disease and proliferative immune-complex GN. We present the case of a 42-year-old Caucasian male with HIV infection, treatment associated peripheral neuropathy, nephrotic syndrome and progressive renal failure. The initial and subsequent kidney biopsies showed diffuse proliferative glomerulonephritis resembling diffuse proliferative (WHO class IV) lupus nephritis. There was no clinical or serological evidence of systemic lupus erythematosus (SLE). Proteinuria improved with ACE-inhibitors, and renal function remained relatively stable while receiving highly active antiretroviral therapy (HAART). A precipitous decline in renal function to end-stage renal disease followed a brief period of withdrawal from potent antiretroviral therapy during which the viral load rebounded. Considering previously reported cases, it appears that lupus-like nephritis is a rare but well-defined pattern of immune-complex-induced renal injury seen in HIV-infected patients. It appears to be markedly responsive to HAART.
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PMID:Lupus-like nephritis in an HIV-positive patient: report of a case and review of the literature. 1452 82

HIV-1-associated nephropathy (HIVAN) is a major complication of HIV-1 infection with distinct pathologic features. Introduction of the HIV-1 genome into mice results in a renal disease with all of the histologic and clinical hallmarks of HIVAN on the FVB/N genetic background (TgFVB). We assessed the influence of genetic background on the development or progression of HIVAN by making F1 hybrids of TgFVB with five other inbred strains (CBA, DBA/2, CAST/Ei, C3H/He, BALB/c) and determining phenotypes relevant to renal failure among transgenic offspring (histology, blood urea nitrogen, proteinuria, serum albumin, and serum cholesterol). We found striking variation in phenotypes among F1s, ranging from severe renal disease to no renal disease whatsoever (P<0.001 for ANOVA across all groups). To map genes responsible for this variation, we produced a backcross of TgFVB/CAST F1 x TgFVB. By genome-wide analysis of linkage in 185 heterozygous transgenic backcross mice, we identified a locus on chromosome 3A1-3, HIVAN1, that showed highly significant linkage to renal disease [logarithm of odds (lod) score 4.9 at D3Mit203, accounting for 15% of the variance in renal disease]. Other loci on chromosomes 11, 14, and 16 were suggestive of linkage to renal disease, and a locus on chromosome 9 influenced serum cholesterol but not nephropathy. Interestingly, HIVAN1 is syntenic to human chromosome 3q25-27, an interval showing suggestive evidence of linkage to various nephropathies. These findings demonstrate a strong genetic influence on HIVAN and demonstrate a major renal disease susceptibility locus on mouse chromosome 3A1-3.
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PMID:Mapping a locus for susceptibility to HIV-1-associated nephropathy to mouse chromosome 3. 1498 36

We describe 7 cases of renal tubular injury in HIV-infected patients receiving an antiretroviral regimen containing tenofovir. Our patients (5 women and 2 men) developed renal tubular dysfunction, with hypophosphatemia, normoglycemic glycosuria, proteinuria, and decrease of creatinine clearance. The first biologic signs of renal toxicity were observed after duration of tenofovir treatment from 5 weeks to 16 months, and they resolved less than 4 months after discontinuation of tenofovir. Six patients had a low body weight (<60 kg). Five patients received low doses of ritonavir, and 1 received didanosine. In 5 patients, the signs resolved with the discontinuation of only the tenofovir. A renal biopsy performed in 1 patient was consistent with tubulointerstitial injury. Proximal tubulopathy appears to be a rare adverse effect of long-term tenofovir therapy. In patients with low weight or mild preexisting renal impairment, regular monitoring of tubulopathy markers could lead to early detection of this dysfunction.
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PMID:Renal tubular dysfunction associated with tenofovir therapy: report of 7 cases. 1507 41

Idiopathic collapsing glomerulopathy is a clinically and pathologically distinct variant of focal segmental glomerulosclerosis characterized clinically by a male and Afro-Caribbean racial predominance, proteinuria (often nephrotic range), and rapid progression to end-stage renal failure. Pathologically, the typical changes are global glomerular collapse leading to obliteration of glomerular capillary lumina, hypertrophy and hyperplasia of podocytes, and severe tubulointerstitial changes. A secondary form with almost identical pathologic features is described in association with human immunodeficiency virus infection. We describe a female patient who presented with multisystemic manifestations, including high spiking fever, arthralgias, lymphadenopathy, striking hyperferritinemia, and impaired renal function with proteinuria. Renal biopsy showed classic collapsing glomerulopathy. A diagnosis of adult Still's disease was made on the basis of Yamaguchi's criteria. The patient was treated with steroids, resulting in remission of the rheumatological condition closely paralleled by remission of proteinuria and renal function, thereby strongly suggesting a causative link between adult Still's disease and collapsing glomerulopathy in this patient. We propose that collapsing glomerulopathy ought to be considered in adult Still's disease with unexplained renal insufficiency or proteinuria.
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PMID:Collapsing glomerulopathy in adult still's disease. 1511 92

A 52-year-old man with 6 years' history of human immunodeficiency virus infection who was receiving highly active antiretroviral therapy presented with acute renal failure and nephrotic syndrome. Renal biopsy revealed features consistent with nephropathy associated with human immunodeficiency virus infection. Treatment consisted of intravenous methylprednisolone followed by oral prednisolone. The patient's renal function improved, although proteinuria persisted. Human immunodeficiency virus-associated nephropathy is very rare in Asian populations and is more common among blacks. To the best of our knowledge, this is the first documented case of nephropathy associated with human immunodeficiency virus infection occurring in Hong Kong.
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PMID:Corticosteroid therapy in a Chinese patient with nephropathy associated with human immunodeficiency virus infection. 1518 Dec 26

In 1984, physicians in New York and Miami reported HIV-infected adult patients with heavy proteinuria and rapid progression to end-stage renal disease. These patients showed large edematous kidneys with a combination of focal segmental glomerulosclerosis (FSGS) and tubulointerstitial lesions. This renal syndrome, named HIV-associated nephropathy (HIVAN), was found predominantly in African Americans. Subsequent studies confirmed the presence of HIVAN in children, who frequently develop nephrotic syndrome in association with FSGS and/or mesangial hyperplasia with microcystic tubular dilatation. Since then, substantial progress has been made in our understanding of the etiology and pathogenesis of HIVAN. This article reviews 20 years of research into the pathogenesis of HIVAN and discusses how these concepts could be applied to the treatment of children with HIVAN. HIV-1 infection plays a direct role in the pathogenesis of childhood HIVAN, at least partially by affecting the growth and differentiation of glomerular and tubular epithelial cells and enhancing the renal recruitment of infiltrating mononuclear cells and cytokines. An up-regulation of renal heparan sulfate proteoglycans seems to play a relevant role in this process, by increasing the recruitment of heparin-binding growth factors (i.e., FGF-2), chemokines, HIV-infected cells, and viral proteins (i.e., gp120, Tat). These changes enhance the infectivity of HIV-1 in the kidney and induce injury and proliferation of intrinsic renal cells. Highly active anti-retroviral therapy (HAART) appears to be the most promising treatment to prevent the progression of childhood HIVAN. Hopefully, in the near future, better education, prevention, and treatment programs will lead to the eradication of this fatal childhood disease.
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PMID:A 20-year history of childhood HIV-associated nephropathy. 1530 Apr 77


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