Life-threatening drug-associated hyperkalemia: a retrospective study from laboratory signals.

PURPOSE: Life-threatening hyperkalemia may be induced by drugs and preventable in at-risk patients. This study was designed to describe cases of 'serious' drug-associated hyperkalemia. METHODS: Adult subjects with a serum potassium concentration above 6.5 mmol/L detected at admission or during hospital stay in nephrology, cardiology, geriatric, emergency or intensive care units were identified by biology laboratories of hospitals and clinics located in Midi-Pyrenees (southwest France). Patients dialyzed for end-stage kidney disease were excluded. Data were collected from medical files. Hyperkalemia was defined as drug-associated if at least one drug known to increase serum potassium concentration was taken when hyperkalemia occurred (among drugs taken in outpatient care for hyperkalemia detected at admission and among drugs taken in outpatient care and continued at hospital and drugs introduced from admission for hyperkalemia detected during hospital stay). RESULTS: Of 168 hyperkalemia cases, 102 (60.7%) were classified as drug-associated. They concerned elderly patients (mean age: 76.1 years) often having arterial hypertension and/or cardiac diseases (88.2%). Risk factors, mainly acute kidney failure, were observed in almost all cases (98.0%). Drugs predominantly involved were angiotensin-converting enzyme inhibitors (47.1%), spironolactone (41.2%), angiotensin II receptor antagonists (23.5%) and potassium supplements (23.5%). In 10% of cases, death could be attributed to hyperkalemia. CONCLUSIONS: Laboratory databases allowed an exhaustive identification of hyperkalemia cases. The frequency of drug-related hyperkalemia and their characteristics suggest that treatment with drugs known to increase serum potassium concentration can be inappropriate, especially regarding associations or indications, and is highly risky for predisposed patients.

[Acute immuno-allergic interstitial nephritis after treatment with fluindione. Seven cases]. / Néphropathie interstitielle aiguë immuno-allergique après traitement par fluindione. A propos de sept cas.

We report seven cases of patients treated with fluindione, who presented with acute renal failure, associated with clinical features of allergy: poor status, fever, dyspnea, lymphadenopathy and erythroderma. All patients had elevated eosinophil counts. Renal biopsy disclosed in all cases a tubulo-interstitial nephritis with or without granuloma. The responsibility of fluindione, an oral anticoagulant widely used in France could be demonstrated. To our knowledge, there are only three reports of single cases of acute renal failure related to fluindione published so far to date. This serious side effect of fluindione should be recognized.

Oxalate nephropathy associated with chronic pancreatitis.

BACKGROUND AND OBJECTIVES: Enteric overabsorption of oxalate may lead to hyperoxaluria and subsequent acute oxalate nephritis (AON). AON related to chronic pancreatitis is a rare and poorly described condition precluding early recognition and treatment. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: We collected the clinical characteristics, treatment, and renal outcome of 12 patients with chronic pancreatitis-associated AON followed in four French renal units. RESULTS: Before AON, mild to moderate chronic kidney disease was present in all patients, diabetes mellitus in eight (insulin [n = 6]; oral antidiabetic drugs [n = 2]), and known chronic pancreatitis in only eight. At presentation, pancreas imaging showed gland atrophy/heterogeneity, Wirsung duct dilation, calcification, or pseudocyst. Renal findings consisted of rapidly progressive renal failure with tubulointerstitial profile. Acute modification of glomerular filtration preceded the AON (i.e., diarrhea and diuretics). Increase in urinary oxalate excretion was found in all tested patients and hypocalcemia in nine (<1.5 mmol/L in four patients). Renal biopsy showed diffuse crystal deposits, highly suggestive of oxalate crystals, with tubular necrosis and interstitial inflammatory cell infiltrates. Treatment consisted of pancreatic enzyme supplementation, oral calcium intake, and an oxalate-free diet in all patients and renal replacement therapy in five patients. After a median follow-up of 7 months, three of 12 patients reached end-stage renal disease. CONCLUSION: AON is an under-recognized severe crystal-induced renal disease with features of tubulointerstitial nephritis that may occur in patients with a long history of chronic pancreatitis or reveal the pancreatic disease. Extrinsic triggering factors should be prevented.

Fatal Yersinia enterocolitica biotype 4 serovar O:3 sepsis after red blood cell transfusion.

BACKGROUND: Although posttransfusion bacterial sepsis is rare, this complication is associated with a high mortality rate. CASE REPORT: A fatal case of septic shock was observed in a 71-year-old patient following transfusion of contaminated red blood cells (RBCs) for refractory anemia. Yersinia enterocolitica was isolated from the patient's blood sample and the transfused RBCs. Both strains were of bioserotype 4/O:3 and had the same NotI pulsotype. High titers of antibodies against Y. enterocolitica were detected in the donor's plasma sample 1 month after blood donation. The donor reported abdominal discomfort 3.5 months before blood collection but had no clinical signs of intestinal infection at the time of donation. CONCLUSION: Y. enterocolitica has been identified with increased frequency as a causative agent of posttransfusion septic shock. This nationwide investigation of these cases led to an estimated incidence of one case per 6.5 million RBC units distributed in France. Although rare, this often fatal complication remains nonpreventable worldwide owing to the lack of practical means for screening RBCs before transfusion.