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Weight loss at a high cost: Orlistat-induced late-onset severe kidney disease.
Buysschaert, B, Aydin, S, Morelle, J, Hermans, MP, Jadoul, M, Demoulin, N
Diabetes & metabolism. 2016;(1):62-4
Abstract
AIM: This report describes a case of kidney failure secondary to orlistat, a lipase inhibitor commonly used in the treatment of obesity. CASE REPORT An 80-year-old man with type 2 diabetes who was being treated with orlistat developed rapidly progressive kidney failure. Low-grade albuminuria argued against diabetic nephropathy. Renal biopsy showed tubulointerstitial nephritis associated with numerous calcium oxalate crystals. Enteric hyperoxaluria was attributed to the orlistat treatment. The latter was stopped and the patient received calcium supplements. Six months after orlistat withdrawal, oxaluria was normalized and kidney function stabilized. CONCLUSION Oxalate nephropathy may result from hyperoxaluria secondary to orlistat treatment. This suggests that kidney function and oxaluria be closely monitored in patients taking orlistat.
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Transient renal dysfunction with reversible splenial lesion.
Watanabe, T, Matsuda, T, Kitagata, R, Tajima, I, Ono, H, Hirano, K, Shirai, M, Endoh, A, Hongo, T
Pediatrics international : official journal of the Japan Pediatric Society. 2014;(5):e68-71
Abstract
We report the case of a 6-month-old boy with transient renal dysfunction who had an intensified signal in the splenium of the corpus callosum on magnetic resonance imaging. He presented to hospital with fever and sudden disturbance of consciousness. Cerebrospinal fluid analysis did not show pleocytosis. The mild consciousness disturbance disappeared after 30 min, but the splenial signal persisted even after 8 days. Further, renal glucosuria, increased excretion of select amino acids, and abnormal fractional excretion of electrolytes were observed, indicating renal tubular dysfunction. The abnormal urinary findings spontaneously resolved by day 9 of hospitalization. The splenial lesion took 21 days to normalize. There were no signs of neurological complications 2 months later. This case suggests the possibility of renal involvement in splenial lesions.
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[Morphological analysis of bone dynamics and metabolic bone disease. Renal Osteodystrophy and New KDIGO CKD-MBD classification].
Tsukamoto, Y
Clinical calcium. 2011;(4):593-7
Abstract
Global Kidney Disease Guideline Organization ; KDIGO has decided to express the abnormality in bone and mineral metabolism associated with chronic kidney disease (CKD) as CKD-Mineral Bone Disorder (CKD-MBD) . The term "renal osteodystrophy" is now only used for expressing bone pathological abnormality diagnosed by biopsy. The classical classification of bone pathology in CKD is superseded by new T (Turnover) M (mineralization) V (Volume) classification.
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[Renal salt-wasting syndrome progressing to severe hyponatremia after chemotherapy--a case report].
Suzuki, H, Hirashima, T, Kobayashi, M, Sasada, S, Okamoto, N, Morishita, N, Tamiya, M, Matsui, K, Kusunoki, Y, Kawase, I
Gan to kagaku ryoho. Cancer & chemotherapy. 2010;(3):543-6
Abstract
A 66-year-old woman with small-cell lung cancer was administered chemo-radiotherapy consisting of cisplatin (CDDP) and etoposide (ETP). From day 3, she developed vomiting and hyponatremia that persisted despite fluid infusion and cortico-steroid administration. On day 7, the hyponatremia worsened (serum sodium level, 109 mEq/L), leading to disturbed consciousness and convulsions. The serum sodium level gradually increased after intravenous administration of hypertonic saline; on day 22, the serum sodium level was almost normal without any neurological implication. We diagnosed this clinical condition as renal salt-wasting syndrome (RSWS) on the basis of dehydration and high urinary sodium excretion at the onset. In the second course of chemotherapy, CDDP was replaced with carboplatin (CBDCA); consequently, hyponatremia was not observed. Hyponatremia that develops after the administration of CDDP may be due to not only the syndrome of inappropriate secretion of anti diuretic hormone (SIADH) but also RSWS. When RSWS is suspected, hypertonic saline should be administered.
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The management of diabetic neuropathy in CKD.
Pop-Busui, R, Roberts, L, Pennathur, S, Kretzler, M, Brosius, FC, Feldman, EL
American journal of kidney diseases : the official journal of the National Kidney Foundation. 2010;(2):365-85
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Abstract
A 64-year-old male with a 15-year history of poorly controlled type 2 diabetes and a 10-year history of hypertension and hyperlipidemia had developed multiple diabetes-related complications within the last 5 years. He first developed albuminuria 5 years ago, and over the next several years experienced fairly rapid decline in kidney function, with eGFR of 55 mL/min/1.73m2 noted 2 years ago. He was diagnosed with proliferative retinopathy 5 years ago and underwent laser photocoagulation. Four years ago, he noted symptoms of peripheral neuropathy manifested as shooting pain and numbness with loss of light touch, thermal and vibratory sensation in a stocking distribution. Last year he developed a non-healing ulcer on the plantar aspect of his left foot which was complicated with gangrene and resulted in a below-the-knee amputation of the left leg one year ago. He now reports a new onset of weakness, lightheadedness and dizziness on standing that affects his daily activities. He reports lancinating pain in his right lower extremity, worse in the evening. Medications include: neutral protamine Hagedorn insulin twice daily and regular insulin on a sliding scale, metoprolol 50 mg/d, lisinopril 40 mg/d, atorvastatin 80 mg/d, furosemide 40 mg/d and aspirin 81 mg/d. Blood pressure is 127/69 mm Hg with a pulse rate of 96 bpm while supine and 94/50 mmHg with a pulse rate of 102 bpm while standing. Strength is normal but with a complete loss of all sensory modalities to the knee in his remaining limb and up to the wrists in both upper extremities, and he is areflexic. Today's laboratory evaluations show a serum creatinine of 2.8 mg/dl, an estimated GFR (eGFR) of 24 ml/min/1.73m2, a hemoglobin A1c (HbA1c) of 7.9 % and 2.1 g of urine protein per gram of creatinine. What would be the most appropriate management for this patient?
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Obesity management in adults with CKD.
Kramer, H, Tuttle, KR, Leehey, D, Luke, A, Durazo-Arvizu, R, Shoham, D, Cooper, R, Beddhu, S
American journal of kidney diseases : the official journal of the National Kidney Foundation. 2009;(1):151-65
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A 22-year-old African-American woman who has been dialysis dependent for four months due to hypertensive kidney disease is referred for kidney transplantation evaluation. Due to the recent occlusion of her left forearm arteriovenous graft, she is currently being dialyzed via a right internal jugular tunneled catheter. Her medications include methyldopa 250 mg bid, Tums 1000 mg with each meal and erythropoietin with dialysis. The patient is single without children, unemployed and lives with her 38 year old mother. She does not smoke or drink. Her review of systems is unremarkable. On physical exam, her weight is 284 pounds, height is 5 feet 2 inches and her body mass index is 51.9 kg/m2. The blood pressure is 130/80 and the cardiac and pulmonary exams are unremarkable. The surgeon feels she is otherwise a good candidate for transplantation except she must lose weight before being listed. What advice should she be given regarding weight loss?
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Monitoring renal function in hypertension.
Martin, U, Coleman, JJ
BMJ (Clinical research ed.). 2006;(7574):896-9
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Abstract
Several classes of antihypertensive drugs can cause a fall in glomerular filtration rate and a rise in serum potassium and creatinine concentrations. Appropriate monitoring during treatment of hypertension allows potentially serious underlying conditions to be identified and adverse events avoided.
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Reversible myopathy and renal impairment.
Freeston, J, Gough, A
Journal of the Royal Society of Medicine. 2004;(3):124-5
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[Radioconstrast nephropathy].
Durdević-Mirković, T, Curić, S, Vodopivec, S, Mitić, I, Bozić, D, Petrović, L, Ilić, T
Medicinski pregled. 2002;(7-8):333-6
Abstract
INTRODUCTION Hospital-acquired acute renal failure increased in the last years from about 5 to 6.4%, while mortality remained high and according to newest investigations it is about 60% on average. Radiocontrast-induced nephropathy is the third cause of death in hospital-acquired acute renal failure. RISK FACTORS FOR RADIOCONTRAST-INDUCED NEPHROPATHY Risk factors for radiocontrast-induced nephropathy include: the existing kidney disease, diabetes, dehydratation, multiple myeloma, older age and earlier kidney damage by contrast substances. COURSE OF RADIOCONTRAST-INDUCED NEPHROPATHY The clinical course of radiocontrast-induced nephropathy may manifest from asymptomatic picture to development of oliguric form of acute renal failure. PREVENTION AND TREATMENT MODALITIES OF RADIOCONTRAST-INDUCED NEPHROPATHY Modalities of prevention and treatment of radiocontrast-induced nephropathy are as follows: adequate hydration of patients, appropriate application of diuretics, calcium channel blockers nonionizing radiocontrast and preventive haemodialysis. EXPERIMENTAL STUDIES IN PREVENTION AND TREATMENT OF RADIOCONTRAST-INDUCED NEPHROPATHY Experimental studies indicate application of atrial natriuretic peptide, endothelin, prostaglandin. CASE REVIEW Two patients treated at the Clinic for Nephrology and Clinical Immunology in Novi Sad, presented with radiocontrast-induced nephropathy. In one patient it appeared after panaortography and in the second after computerized tomography of the abdomen. In both cases aggravation occurred due to already existing renal failure caused by radiocontrast substances. CONCLUSION The problem is particularly important because there is a large number of patients in whom there is a risk of radiocontrast-induced nephropathy and it is necessary to carry out adequate prophylaxis and accurate assessment of kidney function before application of radiocontrast substances.