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Acute interstitial nephritis with severe acute renal failure is reported following tetracycline treatment in a 22-year-old male medical student. Acute renal failure developed within 48 h of a single repeated tetracycline dose and presented 2 days after taking the drug when there was oliguria, nausea, vomiting and bilateral loin pain without rash and fever. The serum creatinine concentration was 8.6 mg/dl and blood urea nitrogen 84 mg/dl. Examination of the urinary sediment revealed 15-20 RBCs per high-power field, and occasional granular and hyaline casts. Percutaneous renal biopsy performed immediately after admission revealed acute interstitial nephritis with immune complexes along the tubular basement membrane and intact glomeruli and was consistent with type 2 interstitial nephritis. Within 4 days of commencement of steroid treatment and hemodialysis, the urine output started to increase with improvement in serum creatinine and BUN levels and after 2 weeks of therapy hemodialysis was discontinued. He remains well 1 year following his illness with complete normalization of his renal function. Although a number of renal side effects of tetracycline antibiotics have been reported, acute interstitial nephritis is rarely caused by tetracycline treatment having been reported just twice following systemic use of minocycline.
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PMID:Tetracycline-induced acute interstitial nephritis as a cause of acute renal failure. 988 23

We report the case of a 21-year-old man who had been developing acute renal failure with Methicillin-resistant Staphylococcus aureus (MRSA) colitis and sepsis. He was admitted for consciousness disturbance, nausea, vomiting, and diarrhea. Oliguria was also observed and his serum creatinine level was elevated to 10 mg/dl. Urinary protein was positive and an abundance of hyaline cast were seen in urinary sedimentation. Diarrhea and pyrexia were prolonged and serum C-reactive proteins were elevated, but lymphocyte and leukocyte counts temporarily decreased from the 3rd to the 6th hospital day and remained low until normalizing after the 14th day. His clinical symptoms improved with hemodialysis (HD) and effective antibiotic therapies. An MRSA strain producing toxic shock syndrome toxin-1 (TSST-1), a super antigen which specifically stimulates human V beta 2-positive T cells, was separated from his feces and blood. To ascertain the cause of his renal dysfunction, a renal biopsy was performed on the 8th day. His renal histology revealed acute interstitial nephritis with severe inflammatory cell infiltration around the medullary areas without glomerular changes. Most of the infiltrated cells were small monocytes, and lymphoid cells were rich in the interstitium. With immunohistochemical staining, over 70% of T-cells were V beta 2-positive. TSST-1-producing MRSA was detected in his blood specimen. Furthermore, V beta 2-positive T cells were accumulated in the renal intersititium, and transient lymphocytopenia was observed. These data suggested the following possible pathogenesis for interstitial nephritis: TSST-1 acts as a super antigen in the renal interstitium where major histocompatibility complex (MHC) is class-2-positive, thereby resulting in interstitial nephritis with T cell migration.
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PMID:[A case of interstitial nephritis induced by a super antigen produced by methicillin-resistant Staphylococcus aureus (MRSA) presenting as acute renal failure]. 1036 25

Two reports of patients with rhabdomyolysis are described. Patient 1 was a 4-year-old-girl who had a 48-hour history of pyrexia and a 24-hour history of vomiting, drowsiness, polydipsia oliguria, and back pain. She could not walk easily because of tenderness in the calves. She was treated with furosemide and dopamine. On day 9, she was mobilized with the aid of physiotherapy. After 2 years, she tired easily but could walk normally. Patient 2 was a 3-year-old girl who had a 24-hour history of general malaise, peripheral aches and pain, and increasing drowsiness. She had severe swelling in the calves. Full-leg four compartment fasciotomies were performed on both calves. After patient 2 healed, she was observed to have muscle regeneration, which is very rare.
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PMID:Catastrophic familial rhabdomyolysis: compartment syndrome with muscle fiber regeneration. 1070 5

BACKGROUND: Although unusual, but not rare, obstruction in the vicinity of the jejunojejunostomy in Roux-Y gastric bypass (RYGBP) can progress in a very short period of time to a life-threatening situation. METHODS: Over a 10-year period in 1,174 RYGBPs, we have seen seven instances of acute and subacute partial to complete small bowel obstructions in the vicinity of the jejunojejunostomy, which can lead to acute gastric dilatation due to obstruction of the bilio-pancreatic limb. Signs and symptoms of the obstruction may include tachycardia, oliguria, hypotension, severe epigastric pain with or without a palpable mass in the epigastrium, chronic bile regurgitation and bilious vomiting, and a possible increase in serum amylase. Laboratory data otherwise has not been helpful, and although a palpable abdominal mass may be diagnostic, the best tools have been radiologic, i.e. the acute abdomen series, limited upper GI series in the patients that appear to be only partially obstructed, abdominal ultrasound and probably most importantly, CT of the abdomen. RESULTS: In the seven cases presented, diagnoses included internal hernia, adhesions, an idiopathic spontaneous hematoma of the bowel wall and retrograde intussusception at the jejunojejunostomy. CONCLUSIONS: Since many surgeons who perform bariatric surgery are alone in their community, they should train their non-bariatric surgical colleagues and associates to be aware of these potential deadly problems.
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PMID:Biliopancreatic Limb Obstruction in Gastric Bypass at or Proximal to the Jejunojejunostomy: A Potentially Deadly, Catastrophic Event. 1072 97

In literature, there was little data about frequency and outcome of ARF with two or more causes in etiology. Therefore, the aim of this study was to search this issue. This series included 339 patients with ARF from Jan 1,1987 to Jan 1,1999. Fourty-six (30 males) of all patients (13.5%) had two or more causes in etiology of ARF. Of these patients, causes were prerenal and renal in 26 (56%), prerenal, renal and postrenal in 12 (26%), renal and postrenal in 4 (9%), and prerenal and postrenal in 4 (9%). The most frequent cause is diarrhea and vomiting in prerenal, gentamycin usage in renal and prostate hypertrophy in postrenal. Of these patients, there was oliguria in 32 (70%), anuria in 8 (17%) and non-oliguria in 6 (13%). Treatment modalities of patients was only medical in 19 (41%), dialysis in addition to medical therapy in 27 (59%). In spite of treatment, 5 (10.8) of patients with two or more causes in etiology died. Causes of death were uremic coma in 2, cardiac disorders in 2 and septic shock in 1. Three (11.2%) of other patients with one cause died. Mortality rates were not different (chi2: 0.0298, p > 0.5). Cortical necrosis was diagnosed in one patient with multiple etiology and 2 of other patients. Finally, frequency of ARF with two or more etiologic causes was 13.5%, and most frequent causes were hypovolemia and nephrotoxic drugs. Outcome of these patients was similar to other patients with one cause.
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PMID:Frequency and outcome of patients with acute renal failure have more causes than one in etiology. 1090 Nov 83

We report tamoxifen-induced hypertriglyceridemia and asymptomatic acute pancreatitis in a 51 year-old women with type 2 diabetes mellitus and stage III-b infiltrative ductal carcinoma, admitted to the hospital with weakness, oliguria and glucose dysregulation. On admission, there was no fever, abdominal or back pain, rebound tenderness, nausea, or vomiting. Following 1 year of tamoxifen treatment, triglycerides increased from 400 to 1344 mg/dl (blood urea nitrogen 52 mg/dl, creatinine 2.0 mg/dl, glucose 341 mg/dl). Hypertriglyceridemia was considered to be due to either diabetic dyslipidemia and/or tamoxifen. On computerized tomography, pancreatic enlargement, heterogenity, hypodensity and a pancreatic pseudocyst (5 x 7.5 cm diameter) were found. Acute pancreatitis was suspected, and serum amylase level was found to be increased (273 IU/L). Tamoxifen was discontinued and gemfibrozil was started. Triglycerides decreased to 301 mg/dl and amylase decreased to 66 IU/L a week later and remained normal thereafter. This case indicates that tamoxifen-induced hypertriglyceridemia may cause acute pancreatitis without classical symptoms which might be due to autonomic neuropathy in diabetic patients. Effects on lipid metabolism should be considered and triglycerides should be closely followed in patients on tamoxifen.
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PMID:Asymptomatic acute pancreatitis due to tamoxifen-induced severe hypertriglyceridemia in a patient with diabetes mellitus and breast cancer. 1212 Aug 88

Ovarian hyperstimulation syndrome (OHSS) is a potentially fatal condition associated with the use of ovulation-inducing drugs. We describe a 28-year-old woman who presented with ascites, oliguria and vomiting. Over 2 weeks, the combination of intractable vomiting, intravenous rehydration, paracentesis, hypercatabolism and proteinuria led to severe hypoalbuminaemia with gross oedema and progressively worsening liver function. The patient's albumin dropped to 9 g/l with liver function abnormalities peaking at: alanine aminotransferase, 462 IU/l; alkaline phosphatase, 706 IU/l; bilirubin, 26 micromol/l; and prothrombin time, 19 s. The judicious use of paracentesis and commencement of total parenteral nutrition coincided with a rapid clinical improvement. One month after discharge, the patient was asymptomatic with normal liver function. This case demonstrates the severity of malnutrition and liver dysfunction that can occur with severe OHSS. Increasing use of in-vitro fertilization techniques makes it mandatory for clinicians to be aware of the clinical features, complications and treatment of this condition, and we would suggest that patients with severe OHSS should be jointly managed by physicians and obstetricians.
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PMID:A severe case of ovarian hyperstimulation syndrome with liver dysfunction and malnutrition. 1216 89

Post-infectious acute glomerulonephritis with hypertensive encephalopathy is characterized by episodic hypertension with headache, vomiting, and hematuria. The association between hypertensive encephalopathy and cortical blindness in children with acute glomerulonephritis is extremely rare. We report the case of a 10-year-old boy with acute glomerulonephritis who presented with gross hematuria, headache, vomiting, and oliguria, and developed transient cortical blindness as a complication of hypertensive encephalopathy. No occurrence of seizure was observed during the clinical course. T2-weighted cranial magnetic resonance imaging showed a high-intensity signal over cortical and subcortical areas of bilateral occipital regions. His vision recovered fully, 2 days after receiving antihypertensive therapy. The patient was well without complaint at 1-year follow-up. This case highlights the possibility that cortical blindness may develop as a complication of acute glomerulonephritis in children. Prevention of the occurrence of neurological deficits in children with acute glomerulonephritis and hypertensive encephalopathy requires careful evaluation and appropriate management of hypertension.
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PMID:Cortical blindness in a boy with acute glomerulonephritis. 1268 14

Familial renal hypouricemia with exercise-induced acute renal failure (ARF) is rare. A 45-year-old man presented with abdominal pain, vomiting, and oliguria after severe exercise. The diagnosis was ARF based on high serum creatinine (SCr) level (5.1 mg/dL [451 micromol/L]). Renal function recovered completely within 2 weeks of conservative treatment (creatinine clearance [Ccr], 100.4 mL/min [1.67 mL/s]). After remission, laboratory results showed serum urate (SUA) of 0.8 mg/dL (48 micromol/L), and fractional excretion of uric acid (FE(UA)) of 46%. The final diagnosis was ARF associated with idiopathic renal hypouricemia. Other diseases that could increase the excretion of urate were excluded. Because only mild responses were observed both in pyradinamide and benzbromarone loading tests, he was considered to be a presecretory reabsorption disorder type. The younger brother (42 years old) also had episodes of low and middle back pain after severe exercise and experienced similar attacks at least 5 times since the age of 29. SCr level was elevated in every attack. Hypouricemia (SUA, 1.0 mg/dL [59 micromol/L]) and high urinary urate excretion (FE(UA), 65.7%) also were detected. Renal function recovered almost completely without any specific treatment. Radiologic examination of the 2 cases showed bilateral urolithiasis probably caused by the high urinary urate excretion. Sequence analysis of a urate anion exchanger known to regulate blood urate level (URAT1 gene) in both brothers showed homozygous mutation in exon 4 (W258Stop), resulting in a premature truncated URAT1 protein. Both their parents and their children showed heterozygous mutation of the URAT1 gene. This is the first report of the 2 male siblings of familial renal hypouricemia complicated with exercise-induced ARF, with definite demonstration of genetic abnormality in the responsible gene (URAT1).
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PMID:Two male siblings with hereditary renal hypouricemia and exercise-induced ARF. 1465 3

Among many viral hemorrhagic fevers, only hemorrhagic fever with renal syndrome (HFRS) occurs in Croatia. HFRS is a natural focus zoonosis with sudden onset, characterized by high fever and other clinical symptoms, renal insufficiency and hemorrhages. In Croatia, HFRS is caused by two types of hantaviruses--Puumala (PUU) and Dobrava (DOB). The basic pathologic and patophysiologic disorder in HFRS is capillary damage (vasculitis). Incubation of HFRS has not been precisely determined, it is most frequently around two weeks. The disease onset is usually abrupt. At the beginning, general symptoms include high fever and myalgias, especially in the lumbar region, and abdominal pain, as well as strong headaches, malaise and nausea, and often vomiting or diarrhea. In half of the patients respiratory symptoms occur. Later on, some patients may experience hypotension, oliguria and other signs of renal failure, and apart from petechial, severe hemorrhages may also occur in other organs. During typical clinical presentation of the disease, some characteristic symptoms are clearly distinguished in particular stages of the disease. Therefore, the course of HFRS is usually divided into five distinct stages (febrile, hypotensive, oliguric, polyuric and convalescent). Such a course of the disease is more commonly present in case of DOB virus than PUU virus infection. The febrile stage with sudden onset usually lasts from 3 to 7 days, when thrombocytopenia and hemoconcentration, as well as albuminuria and hematuria are almost always recorded. The hypotensive stage lasts from one to 2 days on an average and is characterized by lower blood pressure and signs of renal failure. The oliguric stage usually starts at the beginning of the second week of the disease, when extensive hemorrhage may occur and urea and creatinine reach their highest values. The oliguric stage is followed by the polyuric stage which can last for up to two weeks, and is characterized by excretion of a large quantity of urine of low specific gravity (up to 15 liters during 24 hours). The convalescence (convalescent stage) is slower, may last for several weeks or months, but usually resolves without complications. During the infection caused by PUU virus, the course of disease is usually milder with only two stages. The first one is febrile, followed by the second stage with renal symptoms, and rare and mild hemorrhagic manifestations. This type of disease is mostly encountered during epidemics. The mortality in severe cases of the disease (DOB virus) is 5% to 10%, whereas in PUU virus infection it is less than 1%.
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PMID:[Clinical picture of hemorrhagic fever with renal syndrome in Croatia]. 1501 67


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