Intravenous immunoglobulin as adjunctive therapy in kidney transplant recipients with severe pneumocystis pneumonia.

Pneumocystis jirovecii is an opportunistic pathogen that may cause severe, life-threatening respiratory infections in immunocompromised patients such as those with kidney transplants. Although antimicrobial prophylaxis is now universally recommended in the early post-transplant period, Pneumocystis pneumonia (PCP) can occur later. If such infection occurs, mortality rates are high. Beyond standard therapy with trimethoprim-sulfamethoxazole, there is a lack of evidence-based options for intensifying treatment when initial therapy fails to show improvement. Moreover, it is usual to minimize immunosuppression in life-threatening infection, but graft damage may occur, particularly in kidney transplant recipients at above-average immunological risk. Here we present two cases of severe PCP in high immunological risk recipients who were managed with adjunctive intravenous immunoglobulin and withdrawal of immunosuppression. Both patients recovered and were discharged from hospital with functioning grafts.

Male Sexual Dysfunction and Chronic Kidney Disease.

Male sexual dysfunction is common in chronic kidney disease (CKD), particularly in end-stage renal disease. Historically, this cause of considerable morbidity has been under-reported and under-recognized. The ideal approach to diagnosis and management remains unclear due to a paucity of good quality data, but an understanding of the pathophysiology is necessary in order to address the burden of this important complication of CKD. This paper will review the endocrine dysfunction that occurs in renal disease, particularly the hypothalamic-pituitary-gonadal axis, discuss the causes of erectile dysfunction, infertility, and altered body image and libido in these patients and suggest appropriate treatment interventions.

Association of a factor H mutation with hemolytic uremic syndrome following a diarrheal illness.

Hemolytic uremic syndrome (HUS) takes 2 forms: diarrheal HUS and nondiarrheal HUS. As its name suggests, diarrheal HUS classically follows an enteric infection. The classic infective organism is the Escherichia coli O157 serotype, although other bacteria, including Shigella species, can produce the verocytotoxin required to cause HUS. The usual clinical course is an episode of bloody diarrhea followed by thrombotic microangiopathy and acute renal failure. Supportive treatment sees recovery of renal function in the vast majority of patients. Most cases occur in children, but all age groups can be affected. Conversely, nondiarrheal HUS may have one of a number of predisposing factors, including drugs, irradiation, and hypertension. It also is well established that mutations in the genes encoding the complement regulator proteins factor H, factor I, and membrane cofactor protein predispose to nondiarrheal HUS. In patients with nondiarrheal HUS, recovery of renal function is much less common. Here, we present a case of HUS after a diarrheal illness in which the patient did not recover renal function in the long term. A novel mutation in exon 23 of the factor H gene was discovered. This is clinically important. If this patient underwent transplantation, he would be expected to have an 80% risk of graft loss at 2 years because of recurrent HUS. We recommend consideration of complement gene mutations in any patient with HUS after a diarrheal episode in which there are unusual features.