Acute tubular necrosis after renal allograft segmental infarction: the nephrotoxicity of necrotic material. (25/78)

OBJECTIVES: Renal allograft dysfunction can be caused by renal vessel thrombosis, acute tubular necrosis, hyperacute or acute rejection, nephrotoxicity induced by cyclosporine or tacrolimus, thrombotic microangiopathy, or urinary tract obstruction. MATERIALS AND METHODS: We describe a renal transplant recipient in whom oliguria developed during the first week after transplant, although his early renal allograft function was good. RESULTS: A Doppler ultrasonographic study revealed a lack of perfusion in the lower pole of the allograft. A perfusion defect was noted in the lower pole that was supplied by a polar artery, which had been damaged during engraftment. Light microscopy disclosed tubular cell necrosis without evidence of vascular or humoral rejection. CONCLUSIONS: We suggest that toxic molecules such as tumor necrosis factor-alpha released from a segmental infarcted area can induce tubular cell damage and necrosis leading to renal allograft dysfunction.  (+info)

Effects of surgical technique on postoperative renal function after orthotopic liver transplant. (26/78)

OBJECTIVES: The classic technique for orthotopic liver transplant consists of the total excision of the retrohepatic inferior vena cava during native hepatectomy. Controversy about the effects of the classic technique on postoperative renal function continues. The aim of this study was to evaluate the effects of the chosen hepatectomy technique on postoperative renal function. MATERIALS AND METHODS: Of 253 patients who received an orthotopic liver transplant between June 2006 and July 2008 in the Shiraz transplant unit, only 15 underwent operation with the classic technique. Patient demographics and factors including cold ischemic time, warm ischemic time, operative time, transfusions, blood loss, and early postoperative renal function were assessed retrospectively. The criteria for acute renal failure were a serum creatinine level of > 133 micromol/L (1.5 mg/dL), an increase in the baseline serum creatinine level by 50%, or oliguria requiring renal replacement therapy. RESULTS: All patients received a liver from a deceased donor, and none required venovenous bypass during the operation. The minimum mean arterial blood pressure value of the patients during clamping was 65 -/+ 19 mm Hg. The mean preoperative plasma creatinine level was 87.51 -/+ 39.78 micromol (0.99 -/+ 0.45 mg/dL). During the first week after transplant, 7 patients (46.6%) experienced acute renal failure, and 3 of those 7 required renal replacement therapy. By the sixth postsurgical month, 4 of those 7 patients had died (1 from adult respiratory distress syndrome, 2 from sepsis, and 1 from recurrent cholangiocarcinoma). In all other patients, the plasma creatinine level had returned to the normal range by the third postsurgical week 3 or during short-term follow-up. CONCLUSIONS: Use of the classic technique for orthotopic liver transplant may increase the rate of postoperative renal failure, but that complication usually resolves during short-term follow-up.  (+info)

Primary lymphoedema at an unusual location triggered by nephrotic syndrome. (27/78)

INTRODUCTION: Lymphoedema results from impaired lymphatic transport leading to the pathologic accumulation of protein-rich lymphatic fluid in the interstitial space, most commonly in the extremities. Primary lymphoedema, a developmental abnormality of the lymphatic system, may become evident later in life when a triggering event exceeds the capacity of normal lymphatic flow. CLINICAL PICTURE: We present a 3-year-old nephrotic syndrome patient with an unusual localisation for primary lymphoedema. TREATMENT AND OUTCOME: The patient was treated with conservative approach and she was cured. CONCLUSION: In this particular case, lymphoedema developed at an unusual localisation, which has not been recorded before.  (+info)

Avicenna's Canon of Medicine and modern urology. Part IV: Normal voiding, dysuria, and oliguria. (28/78)

Avicenna, the Iranian scientist, describes the mechanisms of normal voiding in his famous book, the Canon of Medicine. Then, he enumerates urinary symptoms. In this article, his discussion on dysuria, its causes, and its pathophysiology is compared with these concepts in modern urology. Avicenna points to some etiologic theories of interstitial cystitis and chronic prostatitis. In the Canon, we can distinguish bases of the theory of infection and mucosal theory, along with abnormalities of urine, psychological factors, and abnormalities in prostatic secretions. Avicenna also indicates some differential diagnoses of and associated disorders with interstitial cystitis. His short but rather concise discussion on oliguria and its causes is an interesting point for urologists and nephrologists.  (+info)

Severe acute renal failure in a patient with diabetic ketoacidosis. (29/78)

Acute renal failure (ARF) is a rare but potentially fatal complication of diabetic ketoacidosis (DKA). Early recognition and aggressive treatment of ARF during DKA may im-prove the prognosis of these patients. We present a case report of a 12 year old female admitted to the hospital with severe DKA as the 1s t manifestation of her diabetes mellitus. She presented with severe metabolic acidosis, hypophosphatemia, and oliguric ARF. In addition, rhabdomyolysis was noted during the course of DKA which probably contributed to the ARF. Management of DKA and renal replacement therapy resulted in quick recovery of renal function. We suggest that early initiation of renal replacement therapy for patients with DKA developing ARF may improve the potentially poor outcome of patients with ARF associated with DKA.  (+info)

Ureteric sludge syndrome. (30/78)

Four cases of a form of obstructive uropathy previously unreported in children are described. All presented with oligoanuria and either flank pain or fluid retention and had evidence of crystalline sludge in their lower ureters. Three cases had an underlying crystalluria.  (+info)

Defining urine output criterion for acute kidney injury in critically ill patients. (31/78)

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Inactivation of Bardet-Biedl syndrome genes causes kidney defects. (32/78)

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