Acute oliguric renal failure in HELLP syndrome: case report and review of literature.

We describe a 32-year-old female with past medical history of preeclampsia, who presented at 29th week of gestation of her second pregnancy with abdominal pain, emesis, and diarrhea. Initial evaluation revealed hypertension, placental abruption, and intrauterine fetal death. After spontaneous rupture of membranes, a stillborn fetus was delivered. The clinical course was complicated by seizures and acute kidney injury requiring hemodialysis. She also exhibited microangiopathic hemolytic anemia, thrombocytopenia, and elevated liver enzymes (consistent with HELLP syndrome). A biopsy showed acute renal cortical necrosis.

Discontinuation of antiretroviral therapy causing progression to end-stage renal disease in an HIV patient diagnosed with immune complex 'lupus-like' glomerulonephritis.

Immune complex 'lupus-like glomerulonephritis' is a type of renal injury seen infrequently in human immunodeficiency virus (HIV) patients and very little is known about the clinical course and treatment. Treatment options are limited but antiretroviral therapy and steroids have been tried with limited success. We report a case of a 21-year-old HIV-positive African American male with lupus-like glomerulonephritis who progressed to end-stage renal disease upon discontinuation of highly active antiretroviral therapy. This case illustrates the importance of antiretroviral therapy as an important treatment modality for immune complex lupus-like glomerulonephritis in HIV patients.

Effect of steroid-free low concentration calcineurin inhibitor maintenance immunosuppression regimen on renal allograft histopathology and function.

BACKGROUND: The most common cause of late kidney transplant failure is insidiously progressive renal dysfunction associated with organ scarring and fibrosis. Advanced donor age, delayed graft function, calcineurin toxicity and repeated acute rejection episodes are risk factors for this pathophysiology. METHODS: We employed 3, 12 and 24 months surveillance renal biopsies, scored using the Chronic Allograft Damage Index (CADI), with periodic estimates of glomerular filtration rate (eGFR) to assess the effect of a steroid-free maintenance immunosuppression regimen on allograft histology and function. Ninety-one patients were induced with Alemtuzumab and then treated with mycophenolate sodium and low trough concentrations of tacrolimus. RESULTS: Fifty-six of 91 patients followed for 24 months showed no clinical rejection and in 16 more only minimal histological or borderline changes as defined by Banff criteria were observed. Histologically acute rejection was observed in 14 patients including two detected on surveillance biopsy. Five patients refused biopsies but showed stable eGFR for 24 months. Graft histopathology in the group with no rejection did not worsen. In contrast, nearly half the patients with acute rejection showed progression of CADI scores and a total of four grafts were lost over the 2 years. The 16 patients with borderline rejection changes exhibited stable glomerular filtration rate throughout, but 12.5% showed progression of CADI scores in the 12- to 24-month period. CONCLUSIONS: Following Alemtuzumab induction and in conjunction with low-dose tacrolimus and mycophenolate, continuous steroid therapy was not required to prevent progressive injury or preservation of graft function in patients without biopsy-proven acute rejection. Scored surveillance renal biopsies provide a useful tool to monitor transplanted kidneys.

Use of anti-CD20 antibody in the treatment of post-transplant glomerulonephritis.

Post-transplant glomerulonephritis (PTGN) accounts for 4-10% of late graft loss. Six consecutive patients who developed PTGN 3-72 months post-transplant presented to our center with deteriorating kidney function and proteinuria. Three had focal segmental glomerulosclerosis; one had membranoproliferative glomerulonephritis Type 1; one recurrent membranous nephropathy; and one recurrent immunoglobin A nephropathy. All six were treated with an aggressive immunosuppression regimen including rituximab, pulse steroids and/or maximization of mycophenolic acid and calcineurin inhibitor therapy. Four of the six patients received plasma exchange. The patients were followed for a minimum of nine months after treatment. Proteinuria decreased from 7.2 ± 4.4 to 1.4 ± 1.5g (p = 0.04), while mean estimated glomerular filtration rate was 31.2 ± 13.1 and 42.5 ± 21.7 mL/min (p = 0.07) at nine months. No adverse events were noted. These observations suggest that immune modulating therapy may be of benefit in the treatment of PTGN.

Lithium-induced membranous glomerulonephropathy in a pediatric patient.

Lithium-induced glomerular toxicity is an infrequent occurrence in pediatric patients. We report a 13-year-old patient presenting with clinical and laboratory evidence of renal insufficiency after long-term lithium use. Biopsy revealed membranous glomerulonephropathy. Discontinuation of the lithium treatment resulted in resolution of the symptoms and laboratory abnormalities. Other alkali metals have been implicated as risk factors for membranous glomerulonephropathy. To the best of our knowledge, this is the first reported case of lithium-induced glomerulonephropathy in a pediatric patient.