Acute cortical necrosis and collapsing glomerulopathy in an HIV-infected patient: A rare clinical scenario

Bakshsish Singh; Ankur Gupta; Sandeep Mahajan; Ruchika Gupta

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LETTER TO THE EDITOR

Year : 2012 | Volume : 23 | Issue : 2 | Page : 363-366

Acute cortical necrosis and collapsing glomerulopathy in an HIV-infected patient: A rare clinical scenario

Bakshsish Singh¹, Ankur Gupta², Sandeep Mahajan¹, Ruchika Gupta³
¹ Department of Nephrology, AIIMS, Delhi, India
² Department of Nephrology, The Ottawa Hospital, Ottawa, Canada
³ Department of Pathology, AIIMS, Delhi, India

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Date of Web Publication

28-Feb-2012

How to cite this article:
Singh B, Gupta A, Mahajan S, Gupta R. Acute cortical necrosis and collapsing glomerulopathy in an HIV-infected patient: A rare clinical scenario. Saudi J Kidney Dis Transpl 2012;23:363-6

How to cite this URL:
Singh B, Gupta A, Mahajan S, Gupta R. Acute cortical necrosis and collapsing glomerulopathy in an HIV-infected patient: A rare clinical scenario. Saudi J Kidney Dis Transpl [serial online] 2012 [cited 2021 Mar 1];23:363-6. Available from: https://www.sjkdt.org/text.asp?2012/23/2/363/93180

To the Editor ,

Involvement of kidneys in patients of acquired immunodeficiency syndrome (AIDS) is well recognized these days. ^[1],[2] The dramatic impact antiretroviral therapy (ART) had on the survival of these patients has led to the development of complications not seen previously, with the spectrum of renal involvement ranging from acute renal failure to chronic renal dysfunction due to nephropathies. ^[2],[3] We present here a 33-year-old lady who presented with human immunodeficiency virus (HIV) and rapidly progressive renal failure and had a rare presentation of the known varied histologies seen in HIV infection.

This patient presented with a history of low-to moderate-grade fever, decreased urine output and shortness of breath for two weeks. There was no associated cough, sputum, chest pain, palpitations, skin rash or joint pains. There was no past history suggestive of any nephrotic or nephritic illness or any uremic symptoms. She was not an intravenous drug abuser. Physical examination revealed pulse 82/min, blood pressure 150/90 mmHg and oral thrush. There was no pedal edema or facial puffiness. Respiratory, cardiovascular, abdominal and central nervous system examinations were essentially normal. Fundus examination did not reveal any changes of hypertensive retinopathy. Laboratory investigations are shown in [Table 1]. Peripheral smear did not reveal any schistocytes. HIV was subsequently confirmed with Western blot analysis.

Table 1: Laboratory parameters at the time of renal biopsy.

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With a clinical diagnosis of rapidly progress-sive renal failure in a HIV-positive patient, a renal biopsy was performed. Renal biopsy tissue processed for light microscopy [Figure 1] showed 11 glomeruli. Two glomeruli showed segmental collapse of the glomerular tuft with hyperplasia and hypertrophy of the overlying visceral epithelial cells. The visceral epithelial cells showed prominent intracellular protein resorption droplets. One fragment showed coa-gulative necrosis of the glomeruli and adjacent tubules without any inflammatory or granulo-matous reaction in the surrounding area. Special stains did not reveal any acid fast bacilli or fungal profiles in the necrotic focus. Some of the small arteries included in biopsy revealed marked fibro-intimal thickening with narrowing of the vascular lumina. One artery, in addition, showed recanalization. Silver-methe-namine stain showed focal disruption of the internal elastic lamina. Arterioles showed hyaline arteriosclerosis. No fibrin thrombi or active vasculitic lesion was detected despite careful search. Immunofluorescence examination showed IgM and C3 in the sclerosed areas

Figure 1: Photomicrographs showing a glomerulus with segmental collapse of the tuft and hyperplasia of overlying visceral epithelial cells (a, H&E ×200). A small core of renal tissue demonstrates focal acute cortical necrosis (b, H&E ×40). One small artery with marked subendothelial fibrocellular hyperplasia and recanalization (c, H&E ×200), better highlighted on silver-methenamine stain (d, ×100).

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.

Her renal functions did not improve and urine output was around 550 mL/day. She was put on chronic peritoneal dialysis and is doing well on it. Physicians recognised kidney involvement by HIV in patients of AIDS in as early as 1984. The disease was invariably fatal until the development of ART in 1996. ART had a dramatic impact on the survival of the patients suffering from HIV disease. But, this has led to development of complications not seen previously due to the increased longevity of these patients. The spectrum of renal involvement in patients infected with HIV is varied, ranging from acute renal failure to chronic renal dysfunction due to nephropathies. Of the latter, an aggressive form of collapsing focal seg-mental glomerulosclerosis (FSGS), referred to as HIV-associated nephropathy (HIVAN), is the classical and the most common histological entity. ^[1] HIVAN, in classic clinical description, is characterized by rapidly progressive renal failure with moderate to nephrotic range pro-teinuria accompanied by bland urine sediment. Although HIVAN was originally described in patients with AIDS, few cases have been reported in asymptomatic HIV infection and after acute seroconversion. ^[2],[3]

Histologically, HIVAN is characterized by changes involving glomerular as well as tubuleinterstitial compartments. The glomerular injury manifests as collapsing FSGS. ^[4] The acute nature of this glomerular injury is evident by lack of appreciable increase in matrix substance. As the lesion evolves, the glomerular tuft solidifies, surrounded by enlarged vacuo-lated visceral epithelial cells. The tubulo-interstitial damage manifests as widespread tubular degenerative and regenerative changes. Distended tubules with loose proteinaceous casts form "tubular microcysts." Accompanying interstitial infiltrate of T lymphocytes and minor proportion of macrophages, plasma cells and B-cells is seen. ^[3] Renal biopsy in our patient showed these characteristic features of HIVAN.

Acute cortical necrosis is a rare and catastrophic cause of acute renal failure, primarily encountered in association with obstetric complications, septicemia, acute pancreatitis, snake bite and, rarely, with hemolytic-uremic syndrome (HUS). ^[5] HUS has recently been described in adult patients with AIDS presenting with acute kidney injury and variable protei-nuria and hematuria. ^[6] The histological appearance of HIV-HUS is similar to that in non-HIV patients, i.e. thrombi in glomerular capillaries, renal arterioles and interlobular arteries with arteriolar endothelial swelling and fibri-noid necrosis. ^[7] Hertig et al reported two patients with AIDS who developed acute cortical necrosis due to HUS. ^[8] Our patient had neither the clinical manifestations of HUS nor the histological evidence of glomerular capillary or arteriolar thrombi. Also, she did not have features of sepsis, although she had history of low-grade fever.

Another cause of microvascular injury in HIV-infected patients is malignant hypertension that has been reported in association with various HIV-associated glomerulonephritis, including collapsing FSGS. In a study by Morales et al, patients with malignant hypertension had grade III hypertensive retinopathy and acute deterioration of renal functions. Renal biopsy showed arteriolar fibrinoid necrosis with inti-mal thickening and luminal narrowing. The presence of malignant hypertension was associated with poor patient and renal survival. ^[9] The renal vascular changes in our patient do not resemble those of malignant hypertension. In addition, severe hypertension and hypertensive retinopathy were absent at the time of renal biopsy.

A wide range of vasculitides have also been reported in HIV-positive patients, including a polyarteritis nodosa (PAN)-like syndrome. PANlike vasculitis, encountered in the HIV setting, differs from classic PAN in the lack of waxing- waning clinical course and rarity of multisystem organ involvement. ^[10] Renal involvement by this PAN-like vasculitis has been reported in only few patients in the literature. ^[11] The vessels involved by PAN-like syndrome in HIV patients tend to be smaller than those in classic PAN, i.e. there is usually pronounced involvement of the microcirculation. ^[12] The clinical behavior of PAN-like vasculitis in HIV-positive patients has been shown to be similar to classic PAN with limited organ involvement. ^[13] The renal histology in our patient resembled the segmental arterial involvement by PAN-like vasculitis, with healing and healed phases and sparing of few vessels.

Our case is the first of its kind of presentation in HIV infection. Dual collapsing glomerulo-pathy and acute cortical necrosis with vasculitis-like picture has never been reported earlier. The case illustrates a varied presentation of HIV. A renal biopsy is warranted in all such cases.^[14]

References

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