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Ovid: Oxford Handbook of Genitourinary Medicine, HIV, and Aids

Editors: Pattman, Richard; Snow, Michael; Handy, Pauline; Sankar, K. Nathan; Elawad, Babiker Title: Oxford Handbook of Genitourinary Medicine, HIV, and Aids, 1st Edition Copyright ©2005 Oxford University Press > Table of Contents > HIV/AIDS > Chapter 48 – HIV: renal disorders Chapter 48 HIV: renal disorders P.472
Introduction Relatively common in those with HIV infection and may just amount to proteinuria (in up to 30%). Necropsy studies in the USA have shown renal pathological abnormalities in 3–7%. Initial presentation may be as acute renal failure, especially in advanced HIV disease, 2° to:

  • Dehydration and electrolyte disturbances (e.g. following vomiting and diarrhoea).
  • Acute tubular necrosis due to:
    • sepsis
    • hypotension
    • drug nephro-toxicity (e.g. tenofovir, adefovir, aminoglycosides, pentamidine, aciclovir, cidofovir, foscarnet, amphotericin B).
  • Obstruction (2° to nephrolithiasis and crystalluria)
    • indinavir—~4% develop nephrolithiasis, prevented by ample fluid intake (>2L a day)
    • sulfadiazine and aciclovir—can cause crystalluria especially in high dosage and with dehydration.

HIV-related 2° infection (e.g. tuberculosis) can involve the kidney but HIV infection itself may cause 1° renal disease. The general management of renal failure should follow the same principles as HIV –ve patients, i.e. fluid/dietary restriction, renal replacement therapy, erythropoietin, vitamin D analogues, etc. HIV-associated nephropathy (HIVAN) First described in 1984. Studies from USA and some European centres suggest that it is the most common HIV-related renal disease. Renal glomerular and tubular epithelial cells have been shown to be infected by HIV, though mechanisms of viral-induced injury are unclear. Predominantly found in black ♂ of African origin and currently the 3rd most common cause of end stage renal disease (ESRD) in African-Americans, aged 20–64 years. Clinical features Presents with nephrotic syndrome—proteinuria >3.5g/day, hypoalbuminaemia, oedema, and hyperlipidaemia. Leads to progressive renal insufficiency. Typically no hypertension. Diagnosis

  • CD4 count is usually <200cells/µL.
  • Urinalysis shows leucocytes, hyaline casts, oval fat bodies but no cellular casts.
  • Renal ultrasound typically shows normal or enlarged renal size with ↑ echogenicity.
  • Definitive diagnosis by renal biopsy showing focal segmental glomerulosclerosis with ‘collapsing’ features and tubular atrophy.

Management Initial reports of dismal prognosis (inexorable progression to ESRD within 6–12 months) have improved with treatment that at least delays disease progression.

  • HAART.
  • Prednisolone (improves renal function by ↓ HIV initiated inflammatory process).
  • Angiotensin converting enzyme inhibitors—treatment of choice for hypertension, but may also be beneficial in the normotensive.

Immune-mediated renal disease Less common than HIVAN but reported as the main cause of HIV-related renal disease in non-African Americans based on studies from France, Italy, and Thailand. Found in 25–50% of those having a biopsy for renal disease. The types of glomerular involvement found include:

  • IgA nephropathy—HIV directly implicated, reported almost exclusively in Caucasians and Hispanics;
  • membranous nephropathy;
  • membranoproliferative, mesangial proliferative, diffuse proliferative, or crescentic glomerulonephritis.

Hepatitis B virus (HBV) and hepatitis C virus (HCV) both more common in injecting intravenous drug users, are important co-infections and may individually cause renal disease. HCV-associated cryoglobulinaemic glomerulonephritis is found in both HIV and non-HIV infected patients but is much more aggressive in the former. Typical presentation includes purpura, arthralgias, and peripheral neuropathy in addition to renal insufficiency. Circulating cryoglobulins and ↓ complement levels may be found. HBV, syphilis, and malignancy may all cause membranous nephropathy and are all found more frequently in those with HIV infection. Clinical features Slowly progressive and mild compared with HIVAN. Typical early features are asymptomatic proteinuria and haematuria (on urinalysis), with mild renal insufficiency. Diagnosis

  • Detection of other infection(s) e.g. syphilis, HBV, and HCV.
  • Renal biopsy.


  • Treat any co-infection or malignancy.
  • HAART.

Interstitial nephritis Not uncommon and may be associated with other renal pathology such as HIVAN. Equal prevalence in blacks and whites. May present with proteinuria, renal failure, or nephrotic syndrome. Acute interstitial nephritis 2° to allergic drug reactions presents with acute renal failure, skin rash, and eosinophilia. Non-steroidal anti-inflammatory drugs are a common cause. P.475
Acute renal failure and HIV seroconversion Acute renal failure and nephrotic syndrome may be presenting features of acute HIV seroconversion. Renal biopsy typically shows acute tubular necrosis and mesangioproliferative glomerulonephritis, with tubuloreticular inclusions. Drugs and renal disease

  • Indinavir: nephrolithiasis, interstitial nephritis
  • Ritonavir: interstitial nephritis
  • Tenofovir: renal tubular dysfunction with hypophosphataemia, normoglycemic glycosuria, and proteinuria. Fanconi’s syndrome and acute renal failure also reported.

Other diseases (less commonly reported) Minimal change disease, amyloidosis, haemolytic uraemic syndrome, and renal malignancy. End stage renal disease Dialysis should be considered (haemodialysis currently the preferred method). May only be required on a temporary basis until HAART is introduced. Cadaver renal transplantation has been performed in small numbers of selected patients with no evidence of ↑ rate of opportunistic infection.

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