Hyperuricemia, unlike clinical gout, is extremely common in renal transplant patients. The high prevalence of hyperuricemia is related to prolonged exposure to cyclosporine rather than to its dose or serum concentration. Serum creatinine levels do not show significant correlation with hyperuricemia, behaving more like a surrogate marker for cyclosporine dose and trough level. The low incidence of gout in renal transplant patients, despite the hyperuricemia, may be related to the prolonged immunosuppression effect.
Heat stroke occurs in the desert area of Saudi Arabia quite frequently and manifest in different patterns including coagulopathy. Frequently encountered complications include renal or hepatic failure, rhabdomyolysis, acute respiratory distress syndrome (ARDS), disseminated intravascular coagulation (DIC), and seizure. Not all of these complications usually occur in the same patient, in case it occurs the mortality reported is significantly high. We describe a case of heat stroke that had nearly all the known complications of heat stroke but recovered from all, except minor neurological deficit in the form of dysarthria and exaggerated deep reflexes.
Our patient was a 40-year-old Indian male, non-smoker non-alcoholic, working as a waiter in a furniture shop in Saudi Arabia. This patient was admitted with a history of nausea, vomiting and generalized weakness of 15 days duration. He had no history of diabetes mellitus, hypertension, renal stone disease or drug abuse. He was afebrile, and his blood pressure was 160/ 100 mmHg standing and 165/102 mmHg lying, with pallor and bilateral pedal edema. Respiratory and cardiovascular examinations were normal. The abdominal examination did not reveal any organomegaly or bruit. The rest of the examination including nervous system and funduscopy was normal. Blood tests showed Hemoglobin-8.2 gm/dl, Hematocrit 24.6% with normocytic normochromic picture, Urea 200 mg/dl, creatinine 14 mg/dl, calcium (Ca) 7.5 mg/dl, Phosphates (Ph) 7 mg/dl, alkaline phosphatase (Alk.Ph) 100 u/l, sodium 140 meq/l, potassium 4.0 meq/l and albumin 4 gm/dl.
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Immunoglobulin A (IgA) nephropathy is the commonest form of primary glomerulonephritis with variable clinical presentation. It has been associated with several infectious and non-infectious diseases but with only few reported cases following traumatic bone fracture. The present case report describes a 55 years old male patient who developed acute kidney injury within 3 months following bone fracture. Urine examination showed microscopic haematuria and proteinuria together with rapid deterioration in renal function. Light microscopic examination of kidney biopsy sections showed glomerular mesangial proliferation with fibro-cellular crescent formation in few glomeruli, two glomeruli were sclerosed, in addition to interstitial inflammation and tubular atrophy. Immunofluorescence microscopy showed mesangial IgA and C3 deposits. The renal function improved substantially following a course of steroids and mycophenolate mofetil without dialysis support. The development of acute IgA nephropathy is possibly followed the incident of traumatic bone fracture.
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