Although acute renal failure is common in patients with fulminant hepatitis, it has been recognized as a rare complication of non-fulrninant acute hepatitis A. So far about 30 patients have been described in the literature who had acute hepatitis A associated with acute renal failure. Variable renal biopsy findings have been described in previous reports, including mostly acute tubular necrosis, mesangial proliferative glomerulonephritis, and interstitial nephritis. But the exact mechanism by which hepatitis A causes acute renal damage is still obscure. We describe two cases with acute hepatitis A, proven by IgM anti-hepatitis A antibodies compli- cated by acute renal failure. One patient required hemodialysis. Kidney biopsy findings showed interstitial nephritis with no evidence of glomerular involvement. Our review of these cases and the relevant literature suggests that there is strong evidence to implicate hepatitis A virus as a cause of acute renal failure. It remains to be elucidated why the histologic features are variable in the cases of hepatitis A virus induced acute renal failure and which factors predispose a patients to have immunologic involvement versus interstitial and tubular involvement.
Acute Kidney Injury ; Antibodies ; Biopsy ; Glomerulonephritis ; Hepatitis A virus ; Hepatitis A* ; Hepatitis* ; Humans ; Immunoglobulin M ; Kidney ; Necrosis ; Nephritis, Interstitial* ; Renal Dialysis

We report one case of renal PV infection after renal allograft transplantation leading to graft dysfunction. According to prior reports, PV induced interstitial nephritis might be a cause of graft loss. Pathologic findings show varying degrees of interstitial infiltration and tubular degenerative changes, which resemble acute cellular rejection. Therapeutic strategies have not yet been developed. Case ; A 23 years old male underwent renal transplantation from his HLA haploidentical 25 year old sister. His renal function had been good with cyclosporin, steroid and azathioprine until 9 months after transplantation, when his serum creatinine level rose to 2.2mg/dl. The renal biopsy revealed diffuse lymphocyte infiltration in the interstitium and feature of the tubulitis. Also, giant tubular epithelial cells with large, hyperchromic nuclei were present. Despite steroid pulsing and OKT3, renal function progressively de- teriorated. After 10 days of OKT3 therapy, the patient suffered from high fever, dyspnea and general aches. A chest X-ray revealed interstitial infiltration in both lung fields and the cytomegalovirus PCR (polymerase chain reaction) test of serum and blood was positive. Intravenous ganciclorvir was administered and immunosuppressants were tapered. 4 months after admission, he lost his graft function and underwent hemodialysis. The aforementioned renal biopsy was retested immunohistochemically. Nuclear inclusions in renal tubular epithelial cells were shown and these inclusions were reacted positively with PV monoclonal antibodies.
Adult ; Allografts* ; Antibodies, Monoclonal ; Azathioprine ; Biopsy ; Creatinine ; Cyclosporine ; Cytomegalovirus ; Dyspnea ; Epithelial Cells ; Fever ; Humans ; Immunosuppressive Agents ; Intranuclear Inclusion Bodies ; Kidney Transplantation ; Lung ; Lymphocytes ; Male ; Muromonab-CD3 ; Nephritis, Interstitial ; Polymerase Chain Reaction ; Renal Dialysis ; Siblings ; Thorax ; Transplants ; Young Adult

A chylous ascites, especially drug-induced, is very rare complication in CAPD. The diagnostic criteria for the drug-induced chylous peritoneal dialysate include 1) turbid dialysate developed within Chrs after the administration of causative drug, 2) no clinical symptoms being suggestive of peritoneal inflammation, 3) the fluid containing normal leukocyte counts and being negative for bacterial and fungal culture, and 4) it disappeared spontaneously after the withdrawal of the assumed causative agent and never recurred thereafter. We report a case of chylous ascites emerging after use of manidipine, dihydropyridine calcium channel blocker, in a patient undergoing CAPD. The chylous ascites in that patient was improved after discontinuation of manidipine.
Calcium Channels ; Chylous Ascites* ; Humans ; Inflammation ; Leukocyte Count ; Peritoneal Dialysis, Continuous Ambulatory*

Liddle syndrome is a rare cause of hypokalemic hypertension and caused by renal tubular sodiurn channel defect resulting in excessive sodium absorption, potassium wasting and metabolic alkalosis. Clinically this syndrome resembles the primary aldosteronism, however, aldosterone and renin secretion are markedly suppressed due to chronic state of volume expansion. This syndrome is transmitted in an autosomal dominant pattern. We have experienced a case of Liddle syndrome, a 74 years old female accompanying severe hypokalemia, long-standing hypertension, metabolic alkalosis and suppressed aldosterone and renin level in serum and urine. She had a history of arrhythmia, torsades de pointes, of unknown cause. We believe that the arrhythmia resulted from severe hypokalemia secondary to this syndrome. Two of her siblings died suddenly, probably from cardio-, cerebrovascular accidents. Five her offspring needed to be evaluated for this syndrome due to its autosomal dominant inheritance. Endocrinologically there was no clue for us to seek other diseases of enzyme deficiency needed in aldosterone synthesis. Once the diagnosis of Liddle syndrome was suspecti, we treated her with amiloride 5mg/day for several days. Thereafter metabolic abnormalities including persistent hypertension, not responded to conventional parenteral potassium replacement and antihypertensive drugs, were reversed and normalized until now. We believe that in some of patients of secondary hypertension of unknown cause, Liddle syndrome should be ruled out, and that the incidence of this syndrome has been underes- timated due to lack of suspicion.
Absorption ; Aged ; Aldosterone ; Alkalosis ; Amiloride ; Antihypertensive Agents ; Arrhythmias, Cardiac ; Diagnosis ; Female ; Humans ; Hyperaldosteronism ; Hypertension ; Hypokalemia ; Incidence ; Liddle Syndrome* ; Potassium ; Renin ; Siblings ; Sodium ; Stroke ; Torsades de Pointes* ; Wills

Spontaneous renal allograft rupture is an uncommon complication of renal transplantation, but it represents a life-threatening emergency that requires prompt recognition and treatment. The incidence of spontaneous renal allograft rupture is variable and range between 3.6 and 9.6 percent of all transplants. In the majority of cases the rupture is associated with acute rejection episodes and with renal vein thrombosis. Most frequently, the allograft rupture occurs within the first 2 weeks of transplantation. in addition, most ruptures reported have occurred in cadaveric renal allograft. Debate on the management of such allograft salvage versus transplant nephrectomy. It appears that the recent trend is toward performing surgical repair of the graft if the rupture is secondary to rejection and oo evidence of renal vein thrombosis ; otherwise, graft nephrectomy be done. We report a case of spontaneous renal allograft rupture due to renal vein thrombosis occurred in a 21-year-old woman 6 days after transplantation. Unusual severe localized pain, swelling over at allograft site, and hypotension, a triad frequently seen in renal allograft rupture, were present. Management by graft nephrectomy was inevitable because of the patient's downhill course.
Allografts* ; Cadaver ; Emergencies ; Female ; Humans ; Hypotension ; Incidence ; Kidney Transplantation ; Nephrectomy ; Renal Veins ; Rupture ; Rupture, Spontaneous* ; Thrombosis ; Transplants ; Young Adult

Phenobarbital is one of long-acting barbiturate with low lipid solubility and used frequently as an anticonvulsant. However, in severe intoxication, hypotension and respiratory arrest are the major causes of prehospital mortality. Mortality is 3M for blood levels over HO pg/mL and estimated lethal adult dose is 6-10g. No effective antidotes are available. We report a case of phenobarbital intoxication in a 29-year-old female, treated successfully with hemodialysis. She was found corhatose on the day of admission and was alleged to have taken 30g of phenobarbital. On physical examination, the blood pressure was 80/60mmHg, and pulse, 97/min. There was no respiration. Pupil was dilated fully. Corneal and deep tendon reflexes were absent. There was no response to painful stimuli. She was treated conservatively with mechanical ventilation, gut decontamination and forced diuresis. Hemodialysis was tried to remove excess phenobarbital for 13 hours. The blood phenobarbital level at admission was 162.2 pg/ mL, which was decreased to 114.4pg/mL after first session of hemodialysis. On the fifth hospital day, blood level decreased to 41.8 pg/mL and she regained her consciousness. She was discharged on the 10th hospital day without major sequelae.
Adult ; Antidotes ; Blood Pressure ; Consciousness ; Decontamination ; Diuresis ; Female ; Humans ; Hypotension ; Mortality ; Phenobarbital* ; Physical Examination ; Pupil ; Reflex, Stretch ; Renal Dialysis* ; Respiration ; Respiration, Artificial ; Solubility

A 35-years-old man was hospitalized with gene-ralized edema. 6 months ago, the patient was operated by radical subtotal gastrectomy for advanced gastric adenocarcinoma. The patient presented with multiple liver metastasis and the massive proteinuria. The patients renal biopsy revealed minimal change nephrotic syndrome and treated with prednisolone and diuretics. The patient was improved clinical symptome and decreased 24 hours urine protein. In literature reviewed, gastric carcinoma was not associated with minimal change nephrotic syndrome. We experienced advanced gastric carcinoma associated with minimal change nephrotic syndrome, thus we report it.
Adenocarcinoma* ; Biopsy ; Diuretics ; Edema ; Gastrectomy ; Humans ; Liver* ; Neoplasm Metastasis* ; Nephrosis, Lipoid* ; Prednisolone ; Proteinuria

Although spontaneous bacterial peritonitis is a frequent complication in the childhood nephrotic syndrome, it is very rare in adults with nephrotic syndrome. It frequently develops when the patients are either in relapse or receiving steroid therapy at the time peritonitis is diagnosed. We report an unusual case of a spontaneous bacterial peritonitis as the presenting feature in a 15-year-old male patient with nephrotic syndrome. He presented with diffuse abdominal pain and distension for 15 days. Abdominal paracentesis revealed the diagnostic laboratory findings of peritonitis, and the bacterial culture of the ascites showed a mixed growth of Escherichia coli and Pseudomonas aeruzinosa. His serum albu- min level was 1.6gldL and the amount of 24 hours proteinuria was 21.0g/day. Although he was treated with adequate antibiotics for 3 weeks, the peritonitis was more aggravated. We decided to insert a catheter into the peritoneal cavity for continuous drainage of the intractable ascites. Two weeks after drainage, the peritonitis improved as the peritonitis subsided, the proteinuria disappeared completely without a steroid therapy. Six months after spontaneous remission, the proteinuria have recurred, and the kidney biopsy then showed focal segmental glomerulorsclerosis.
Abdominal Pain ; Adolescent ; Adult ; Anti-Bacterial Agents ; Ascites ; Biopsy ; Catheters ; Drainage ; Escherichia coli ; Humans ; Kidney ; Male ; Nephrotic Syndrome* ; Paracentesis ; Peritoneal Cavity ; Peritonitis* ; Proteinuria ; Pseudomonas ; Recurrence ; Remission, Spontaneous

Iodinated contrast-induced acute renal failure is estimated to occur in 0.15 to 2% of all patients undergoing contrast imaging studies. Incidence is higher in patients with renal insufficiency, diabetes mellitus, dehydration, multiple myeloma, congestive heart failure, advanced age. We here report successful vascular interventional procedure by using gadopentetate dimeglumine(Gd-DTPA) as a contrast agent in a patient with chronic renal insufficiency and right superficial femoral artery stenosis. The patient had a history of iodinated contrast-induced acute renal failure. Gd-DTPA(0.17mmoVkg) diluted 1: 1 with 0.9% norrnal saline was used as contrast agent for the interventional procedure. Percutaneous transluminal angioplasty was successfully performed and there was no evidence of contrast material- induced acute renal failure after the procedure. Gd- DTPA is an alternative contrast agent for patients with chronic renal insufficiency.
Acute Kidney Injury ; Angioplasty* ; Constriction, Pathologic ; Dehydration ; Diabetes Mellitus ; Femoral Artery ; Gadolinium DTPA* ; Heart Failure ; Humans ; Incidence ; Multiple Myeloma ; Pentetic Acid ; Renal Insufficiency ; Renal Insufficiency, Chronic*

No abstract available.
Kidney ; Kidney Diseases ; Paraproteinemias