Likely Recurrence of C3 Glomerulonephritis in Kidney Transplantation: An Entity to Bear in Mind: Case Report.

BACKGROUND: C3 glomerulonephritis (C3GN) is an unusual entity that is caused by dysregulation and hyperactivity of the alternative complement pathway. Renal biopsy immunofluorescence study shows C3 deposits with absence of immunoglobulins and markers of the classical complement pathway. More than 50% of cases develop end-stage renal disease. Less well-known is the course of C3GN after kidney transplantation. CASE REPORT: We present the case of a 60-year-old woman with chronic kidney disease secondary to chronic glomerulonephritis of unknown origin who received a kidney transplant. Two years later, she presented worsening renal function with non-nephrotic proteinuria and microhematuria. Complement testing revealed low serum levels of C3. Kidney biopsy showed alterations compatible with C3GN that we interpreted as a relapse of the underlying disease.

Transplant glomerulopathy: clinical course and factors relating to graft survival.

INTRODUCTION: Transplant glomerulopathy (TG) is usually associated with a poor prognosis for kidney graft survival. AIM AND METHODS: We analyzed 30 cases of TG diagnosed by kidney biopsy among a retrospective review of 579 biopsies performed between January 2006 and October 2011. RESULTS: At the time of biopsy, the mean glomerular filtration rate (GFR), estimated by the abbreviated Modification of Diet in Renal Disease was 31 ± 10 mL/min and the proteinuria, 1.9 ± 2 gr/24 hours. Anti-human leukocyte antigen (HLA) antibodies were present in 40% of patients. The histological findings showed severe duplication of the glomerular basement membrane in 80% of patients; and interstitial fibrosis and tubular atrophy (IFTA) and moderate to severe arteriolar hyalinosis in 53% and 56% respectively. Fourteen patients lost their grafts. Graft survival was significantly associated with IFTA (P = .03) and renal function at the time of diagnosis (P = .03). CONCLUSIONS: TG was associated with a worse prognosis for the graft among kidney transplant patients. It is often associated with the presence of anti-HLA antibodies. Renal function at the time of diagnosis and IFTA were predictive factors for graft survival in these patients.

Creatinine clearance and proteinuria as early markers of kidney graft survival.

INTRODUCTION: In patients who receive a kidney transplant from expanded criteria donors (ECDs), few studies are available concerning the relation between the clinical characteristics, pretransplant biopsies, and graft outcomes. AIM: To identify early clinical markers predicting worse graft survival in recipients of kidneys from ECDs. MATERIALS AND METHODS: Between 1999 and 2006, we performed a prospective, observational study in 180 recipients of kidney grafts from ECDs that had undergone a preoperative biopsy to evaluate viability. The patients received immunosuppression with basiliximab, late introduction of tacrolimus, mycophenolate mofetil, and steroids. Data were gathered on demographic and posttransplantation clinical characteristics at 1, 3, 6, and 9 months, including estimates of proteinuria and of the glomerular filtration rate using the Modification of Diet in Renal Disease (MDRD) formula. RESULTS: The mean age of the donors was 63.54 years and of the recipients, 58.38 years. A creatinine clearance below the median (40 mL/min, interquartile range 32-50 mL/min) in the first posttransplant year was significantly associated with worse death-censored graft survival (log-rank 14.22, P<.0001). A proteinuria value above the median (100 mg/24 h, interquartile range 40-275 mg/24 h) at 1 year posttransplant significantly reduced the death-censored graft survival (log-rank 14.3, P<.0001). Multivariate Cox analysis showed that a creatinine clearance<40 mL/min in the first year (hazards ratio [HR] 5.7, 95% Confidence Interval [CI] 1.62-20.37; P=.007) and proteinuria at 1 year greater tan 100 mg/24 h (HR 8.3, 95% CI 2.15-32.06; P=.002) were independent risk factors for death-censored graft loss after adjusting for donor age and acute rejection episodes. CONCLUSIONS: Limited renal function and/or low proteinuria at 1 year posttransplant were associated with worse kidney graft survival among recipients of kidneys from ECDS.

[Rhabdomyolysis due to muscle enzyme deficiencies]. / Rabdomiolisis por déficits enzimáticos musculares.

Rhabdomyolysis is a syndrome characterized by injure of skeletal muscle with the release of intracellular constituents into the circulation. Acute renal failure is a common complication and is the leading cause of morbidity and mortality in these patients. The most common aetiology is traumatisms, muscle compressions and extreme exertions. Most commonly, the cause of rhabdomyolysis is evident from the careful clinical history. Nevertheless, when the precipitant is not obvious the diagnosis is difficult and a raised clinical suspicion is required. We should investigate used medication or drugs, infections, electrolyte abnormalities and a number of inherited enzyme deficiencies, in which cases the muscle is unable to use available energy. We report two clinical cases of acute renal failure due to rhabdomyolysis by metabolic myopathies due to a carnitine palmitoyltransferase deficiency on the one hand and by myophosphorylase deficiency on the other. We describe their clinical features and progress.