Malignant hypertension with thrombotic microangiopathy and persistent acute kidney injury (AKI).

Two cases of malignant hypertension presenting with acute kidney injury, thrombocytopenia and hemolytic anemia are presented. In both patients a prolonged duration of renal replacement therapy was required. The plasma levels of ADAMTS13 enzyme were not helpful in delineating the precise pathogenesis in both cases, as the decrements were not severe. We discuss the clinic-pathologic correlation of the biopsy findings and persistence of AKI.

Preeclampsia 2012.

Preeclampsia is a common complication of pregnancy associated with high maternal morbidity and mortality and intrauterine fetal growth restriction. There is extensive evidence that the reduction of uteroplacental blood flow in this syndrome results from the toxic combination of hypoxia, imbalance of angiogenic and antiangiogenic factors, inflammation, and deranged immunity. Women treated for preeclampsia also have an increased risk for cardiovascular and renal disease. At present it is unclear if the increased cardiovascular and renal disease risks are due to residual and or progressive effects of endothelial damage from the preeclampsia or from shared risk factors between preeclampsia and cardiac disease. Moreover, it appears that endothelin-1 signaling may play a central role in the hypertension associated with preeclampsia. In this paper, we discuss emerging data on the pathogenesis of preeclampsia and review therapeutic options.

Pulmonary hemorrhage with hematuria: do not forget IgA nephropathy.

IgA nephropathy is the commonest cause of glomerulonephritis worldwide, and is usually a renal-limited disease. In rare cases, IgA nephropathy may also present with a pulmonary-renal syndrome in which pulmonary hemorrhage is a critical feature. Patients presenting with IgA nephropathy and pulmonary hemorrhage have high morbidity and are at high risk for mortality unless rapid immunosuppressive therapy is instituted. We present a case of IgA nephropathy complicated by pulmonary hemorrhage in which immunosuppressive therapy led to a good outcome, and review the literature on similar cases and the outcome of therapy.

Retroperitoneal fibrosis: a rare cause of acute renal failure.

Introduction. Retroperitoneal fibrosis is a rare cause of acute renal failure (ARF) with only a handful of cases reported in literature. We report a case of a 40-year-old male with an incidental finding of retroperitoneal fibrosis. Case Presentation. Patient is a 40-year-old African American male with no significant past medical history who presented with a four-month history of low back pain and associated nausea with vomiting. Physical examination was significant for elevated blood pressure at 169/107 mmhg and bilateral pedal edema. Significant admission laboratory include blood urea nitrogen (BUN) of 108 mg/dL, serum creatinine (Cr) of 23 mg/dL, bicarbonate of 19 mg/dL, and potassium of 6.2 mmL/L. Renal ultrasound showed bilateral hydronephrosis. Post-void residual urine volume was normal. Abdominopelvic CT scan showed retroperitoneal fibrosis confirmed with fine-needle biopsy. He was treated with a combination of bilateral ureteral stent placement, hemodialysis, and steroid therapy. Four months after hospital discharge, his BUN and Cr levels Improved to 18 mg/dL and 1.25 mg/dL, respectively. Conclusion. Retroperitoneal fibrosis should be considered as a differential diagnosis in patients with acute renal failure and obstructive uropathy. Abdominal CT scan is the examination of choice for diagnosis. Full resolution with treatment depends on the duration of obstruction.

Spontaneous perinephric haemorrhage and acute renal failure in pregnancy due to cocaine intoxication.

Cocaine abuse may contribute to the diverse forms of renal injury. We report a case of a pregnant woman who developed a large subcapsular renal haematoma after cocaine intoxication at 18-week gestation. She stabilized on conservative management and presented again at 29-week gestation with pre-eclampsia, acute renal failure and fetal demise. She required caesarean section delivery and intensive antihypertensive therapy to control severe pre-eclampsia associated with cocaine intoxication. This case is unique in that it is the first report of cocaine intoxication in pregnancy complicated by subcapsular haemorrhage. We discuss the possible mechanisms for the occurrence of this complication.

Hamilton Naki, transplant surgeon.

A biographic sketch of Hamilton Naki is presented here. He was a great self-taught surgeon whose contributions to the world of transplantation were largely ignored due to the apartheid system of South Africa. He assisted Christian Barnard in the first human heart transplant in 1967.

Predictors of outcome in hospitalized patients with severe hyponatremia.

UNLABELLED: Severe hyponatremia is associated with increased morbidity and mortality. Clinicians treating patients with severe hyponatremia are often torn between a desire to promptly raise serum sodium concentration to a "safe range," and at the same time, to avoid excessively rapid correction of hyponatremia. The aim of this study was to assess the prevalence of severe hyponatremia in hospitalized patients, the etiologic factors involved, as well as treatment and outcome of the patients using a retrospective case series. METHODS: Retrospective study of 168 patients with severe hyponatremia (< 115mmol/L) seen at Grady Memorial Hospital, a tertiary teaching hospital, in Atlanta, Georgia, from 1997-2001. The main outcome measures of interest were death during admission or occurrence of neurologic symptoms before, during or after therapy. RESULTS: One hundred sixty-eight patients met the inclusion criteria out of a total of 5994 patients with hyponatremia treated at our hospital over the study period. Eighty-nine patients (52.9%) were symptomatic. The mean absolute serum sodium at 48-hours of therapy was 120.02 +/- 8.31 mmol/L. Respiratory failure and/or hypoxia was present in 28 patients (16.7%); sepsis was documented in 16 patients (9.5%). Mortality rate was high, 34 patients died (20.2%). On multivariate analysis factors with strong association with mortality of patients with severe hyponatremia were hypoxia, presence of neurologic symptoms, slow correction rates and a diagnosis of sepsis. CONCLUSIONS: The mortality associated with severe hyponatremia remains high. Sepsis, respiratory failure and the presence of symptoms predict poor outcome in hospitalized patients with severe hyponatremia. More aggressive therapy with 3% saline may improve outcome in symptomatic patients. Our data suggest that a slow rate of correction in severe hyponatremia is associated with higher mortality than rapid correction, at least in the short-term.

Race and kidney disease: role of social and environmental factors.

Numerous studies have documented the presence of racial disparities among Americans in health outcomes with respect to cardiovascular disease, infant mortality, cancer, and kidney disease. With regard to kidney diseases, these disparities are more dramatic. African, Hispanic, and Native Americans have the highest risks of end-stage renal disease (ESRD). The incidence of ESRD is four times higher in African Americans than in whites. Diseases causing chronic kidney failure, such as diabetes mellitus, hypertension, systemic lupus erythematosus, and human immunodeficiency virus-associated nephropathy, are particularly prevalent among African-American patients. In addition to the higher prevalence, the morbidity associated with kidney complications of these diseases appears worse in African-American patients. African Americans also have worse outcomes and a relatively reduced access to kidney transplantation--the best therapy for ESRD. It is highly likely that social and environmental factors play a very significant role in the persistence of these disparities. A detailed understanding of these socioeconomic and environmental factors will be critical in formulating rational public health strategies to redress these disparities. This paper reviews the social, economic and environmental factors that impact on the incidence of ESRD in minority groups.

"Black swan in the kidney": renal involvement in the antiphospholipid antibody syndrome.

The antiphosphospholipid antibody syndrome (APS) describes a clinical entity with recurrent thrombosis, fetal loss, thrombocytopenia in the presence of lupus anticoagulant and/or antibodies to cardiolipin. These antibodies may be associated with connective tissue diseases such as systemic lupus erythematosus (secondary APS) or be found in isolation (primary APS). Renal syndromes increasingly being reported in association with these antibodies include thrombotic microangiopathy, renal vein thrombosis, renal infarction, renal artery stenosis and/or malignant hypertension, increased allograft vascular thrombosis, and reduced survival of renal allografts. Although much has been understood concerning the biology of these antibodies and the pathogenesis of thrombosis, the optimal therapy remains to be elucidated. This article presents a historical review of the renal involvement in the antiphospholipid syndrome and discusses therapeutic options. Further research is needed.

Celecoxib-induced acute interstitial nephritis.

Data about the nephrotoxicity of selective cyclooxygenase-2 inhibitors are still evolving. Acute interstitial nephritis is a well-described complication of therapy with nonselective nonsteroidal anti-inflammatory drugs. We report a case of biopsy-proven acute interstitial nephritis in a 73-year-old diabetic woman, who had taken celecoxib for more than 1 year before presentation. She presented with clinical findings of subnephrotic proteinuria and acute renal failure that required dialysis. She recovered renal function with cessation of celecoxib therapy after 2 weeks. Other medications were reintroduced safely, without recurrence of renal failure. A kidney biopsy specimen showed acute interstitial nephritis with a prominent eosinophilic infiltrate in the interstitium. This case documents the occurrence of acute interstitial nephritis with celecoxib and emphasizes the need for continued vigilance and care in use of cyclooxygenase-2 inhibitors in high-risk patients.

How to prevent, recognize, and treat drug-induced nephrotoxicity.

Many drugs can injure the kidneys, but they cause renal injury via only a few common mechanisms. Many patients who develop renal injury after drug exposure have identifiable risk factors that could be modified or that should preclude the use of these drugs in the first place.