Infections and the kidney [link]
Any infection causing septicaemia can cause acute kidney injury (AKI), the commonest being meningococcal septicaemia. Acute post-infectious glomerulonephritis and urinary tract infection (UTI) are described in Chapter 4, [link] and Chapter 9, [link]. This chapter describes infections that specifically affect the kidneys.
The general principle in all infection-associated renal complications is that treatment should be aimed at the underlying infection. Eradicating or suppressing the underlying infection is usually the best treatment for the associated renal disease.
• Most have active hepatitis B infection (HBsAg and HBeAg positive) without antibodies, although core antibody may be present.
• Remission occurs with disappearance of the HBeAg and development of hepatitis B (HB) surface antibodies.
• No kidney-specific treatment is of proven benefit.
• HB surface antigen positive children being considered for renal transplantation require assessment by a paediatric hepatologist. Untreated active viral replication, chronic active hepatitis or cirrhosis has a poor prognosis post-transplant.
• Has been associated with glomerulonephritis of various types. The commonest is membranoproliferative glomerulonephritis (MPGN) associated with cryoglobulinaemia. Hepatitis C virus (HCV) leads to chronic overstimulation of B-lymphocytes and production of mixed cryoglobulins that are deposited in the mesangium and glomerular capillaries.
• Antiviral therapy includes interferon-alpha and ribavirin (seek expert advice). Long-term prognosis depends on sustained HCV RNA clearance from serum at least 6 months after cessation of therapy, but no treatment is of proven benefit to the kidney outcome.
• Hepatitis C positive children being considered for renal transplantation require assessment by a paediatric hepatologist. Survival post-transplantation is improved compared with remaining on dialysis.
Human immunodeficiency virus
• HIV-associated nephropathy (HIVAN) is defined by the presence of proteinuria associated with mesangial hyperplasia and/or global-focal segmental glomerulosclerosis, in combination with microcystic transformation of renal tubules. Glomerular capillary collapse associated with hyperplasia of podocytes (collapsing glomerulopathy) may also occur.
• Alternatively there may be mesangial proliferative lesions secondary to immune complex deposits and lupus-like changes.
• African Americans show a unique susceptibility to develop HIVAN.
• Treatment is with antiretroviral therapy.
• Renal transplantation in adults has been successful, provided there is stable maintenance of anti-retroviral therapy, the HIV viral load is undetectable for at least 6 months, and the CD4 cell count is greater than 200cells/mm3.
• Plasmodium falciparum can cause AKI as malarial parasites in red blood cells affect their circulation in the renal microvasculature.
• Plasmodium malariae infections can be associated with nephrotic syndrome, also called quartan malaria nephropathy; however, a direct causal link has not been demonstrated, and neither antimalarial therapy nor steroid therapy are effective.
• Infection is through skin contact with the urine of infected animals.
• Presentation is with fever, muscle pain, conjunctivitis, and in severe cases, renal and liver failure.
• Organisms invade the renal tubules and can be found in the urine.
• Treatment is with penicillin and tetracyclines. Occasionally, steroids are required to treat severe late immunological sequelae (caused by immune complex disease), such as pulmonary haemorrhage after the acute infection is treated.
• Occurs in Asia, Africa, and South America.
• Renal disease is associated with Schistosoma mansoni infection.
• May present with dysuria and terminal haematuria as the worms lay their eggs in the venous plexuses surrounding the bladder and ureters.