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A differential diagnosis of common bacterial peritonitis and appendicitis is difficult in continuous ambulatory peritoneal dialysis (CAPD) patients, and thus the definite diagnosis of appendicitis is often delayed. In this case, a 60-year-old man undergoing CAPD was at first diagnosed with bacterial peritonitis but not appendicitis, and antibiotics were administered. The number of leukocytes in the peritoneal effluent decreased mildly, but the level of C-reactive protein continued to be high and the pain aggravated. When the catheter was removed, suppurative appendicitis was confirmed for the first time. Levels of matrix metalloproteinase (MMP)-2 and -9 in peritoneal effluents were markedly high. Appendicitis should be diagnosed as early as possible because MMPs directly injure the peritoneum via degradation of extracellular matrix proteins. Future studies in a greater numbers of cases of appendicitis are required.

Fabry disease (FD) is a genetic disorder caused by a-galactosidase A gene mutation. Ultrastructural analysis revealing zebra bodies are the typical morphological characteristics. However, certain tricyclic antidepressants and some other medications could induce renal phospholipidosis mimicking FD. We report a 33-year-old man has been taking carbamazepine intermittently for around 10 years whenever he experiences pain and paresthesia in his fingers. He experienced mild edema on both lower limbs half a year ago. Laboratory tests revealed a fluctuating urine protein between + and ++. Electron microscopy revealed laminated “zebra body” in podocytes, which is typical of FD. However, the patient had no family history and the sequencing of the a-galactosidase gene revealed no mutations. The a-galactosidase A enzyme activity was normal at 6.03 μmol/mL/h (normal 2.40–17.65 μmol/mL/h), and low expression of globotriaosylceramide (Gb3) was detected in the renal tissue of this patient. Therefore, the diagnosis of Fabry disease was excluded. Considering the patient’s long-term treatment with carbamazepine (blood level 1.8 μg/ml), we speculated whether the pathological features could be associated with renal phospholipidosis caused by carbamazepine. The follow-up data showed that proteinuria was improved (fluctuated at + ~ −) after discontinuing carbamazepine for six months, which further seemed to support the above diagnosis. Therefore, we concluded that a possible case of carbamazepine-induced renal phospholipidosis, mimicking that observed in FD, has been associated with its nephrotoxicity.

An 84-year-old man was referred to our hospital for atrioventricular block and severe hypokalemia. He had been treated for hypertension since 2007 with indapamide, a thiazide-like diuretic. His laboratory data had not been tested for a long time. One week before his first visit, he suffered from a common cold and anorexia. He was admitted to our hospital because his electrocardiogram showed ventricular flutter, and pulmonary arrest occurred at the time of his visit. Cardiopulmonary resuscitation was successfully performed. Hypokalemia (K, 1.7 mEq/L) was considered as the cause of acute cardiopulmonary failure. His oral intake of potassium decreased, but potassium loss from the kidney persisted (urinary potassium, 14.0 mEq/L; transtubular potassium gradient, 5.00). These results suggested that although hypokalemia was suspected to have been present for a long time due to indapamide, severe hypokalemia was induced during the period of anorexia. After discontinuation of indapamide and intravenous administration of potassium l-aspartate for potassium supplementation, the patient’s serum potassium levels increased and his general condition improved. Although it is well known that hypokalemia is caused by indapamide, the incidence is not frequent and if observed is not severe. However, we experienced an unusual case of hypokalemia-induced fatal arrhythmia caused by indapamide. Hence, the serum potassium concentration of patients under the drug, especially anorexic elderly patients, should be monitored.

Cholesterol crystal embolism (CCE) is caused by the shedding of cholesterol crystals into the bloodstream, and it has been recently recognized as a serious complication after vascular procedures. Our case of CCE, which was diagnosed by skin and renal biopsies, occurred in a patient with hypertension and diabetes mellitus, 3 months after coronary angiography, with the development of renal failure and blue toes. After low-density lipoprotein apheresis (LDL-A), the skin lesions, including livedo reticularis and pain from the acrocyanotic toes, dramatically improved, with partial recovery of renal function. Following the administration of low-dose corticosteroid and candesartan – an angiotensin II type 1 receptor antagonist (ARB) – the eosinophilia disappeared and renal function improved gradually with a decrease in urinary protein excretion. Therefore, a combination therapy of LDL-A, low-dose corticosteroid, and an ARB is a possible treatment for CCE, although the possibility of spontaneous recovery of renal function cannot be eliminated for this patient.

The renal cortex volume is associated with the kidney function and chronic kidney disease (CKD) risk factors, and it may also be a prognostic factor. We aimed to create an equation to estimate the renal cortex volume of CKD patients in day-to-day clinical practice. The subjects included 116 ethnic Japanese CKD patients who were ≥ 18 years of age. The renal size (length, width and thickness) was measured by ultrasound. The body height, weight, year of age, sex, birth weight, gestational age, diabetes status, hypertension status, family history of CKD and dialysis and estimated glomerular filtration rate (eGFR) were collected as expected dependent variables. We made models for the equation regarding the renal cortex volume measured by non-contrast magnetic resonance imaging as a true renal cortex volume. Stepwise multiple linear regression analyses were performed with the log-transformation of dependent and independent variables. The accuracy of the models was compared using the leave one out cross-validation method. The estimated volume of the renal cortex (cm3) = 0.012 × renal length (cm)0.92 × width (cm)0.53 × body weight (kg)0.40 × body height (cm)0.67 × eGFR (ml/min/1.73 m2)0.22 × 1.12 if diabetes. The adjusted R 2 value and the accuracy within 30 and 50% were 0.73, 0.94 and 0.99, respectively. This study provided a new method for estimating the renal cortex volume in day-to-day clinical practice.

Membranous nephropathy (MN) is one of the most common causes of nephrotic syndrome in adults. The J-RBR/J-KDR registry developed by the Japanese Society of Nephrology provides nationwide cohort data for epidemiological studies of MN. MN was present in 36.8% of 1,203 primary nephrotic syndrome patients in Japan. In addition, 633 (77.9%) out of 813 MN patients were referred to as “idiopathic,” whereas 22.1% were classified as “secondary” and involved conditions such as systemic lupus erythematosus, drug exposure, infections, cancer, and various collagen diseases. The mean age of the MN patients was 62.2 (2–88) years old, their mean eGFR was 76.7 (7.6–154.6) ml/min/1.73 m2, and 63.3% had hypertension at the time of renal biopsy. On the basis of these findings, half of Japanese idiopathic MN patients have risk factors (age >60, male, or lower eGFR) for end-stage renal failure, and 10% belong to the high-risk group (daily proteinuria of over 8.0 g). Further studies with high-grade evidence should resolve the natural history and therapeutic problems of idiopathic MN in elderly Japanese.