The natural course of native kidneys after hemodialysis initiation in patients with autosomal dominant polycystic kidney disease (ADPKD) remains poorly understood.
We measured the total volumes of native kidneys in 12 patients who had at least one enhanced computed tomography (CT) image both before and after initiation of hemodialysis (group 1) and in 18 patients who had no image before dialysis but more than two images after dialysis (group 2). In patients with images, the last image was used for analysis only after dialysis.
The mean total kidney volume (TKV) (± SD) before hemodialysis initiation was 3132 ± 1413 mL and the mean TKV of the last image was 3047 ± 1323 mL in group 1. The mean TKV change rate (%) was −5.2 ± 27.4% (
The results suggest that the TKV of native polycystic kidneys decreases substantially after hemodialysis initiation. This reduction occurs mainly during the early post-hemodialysis period and followed by a slow enlargement of TKV.
Bartter syndrome is a renal tubular defect in electrolyte transport characterized by hypokalemia, metabolic alkalosis, hyperreninemia, hyperaldosteronism, normal blood pressure, and other clinical symptoms. As a clinical and genetical heterogeneous disorder, this syndrome can be classified into two clinical variants, antenatal Bartter syndrome and classic Bartter syndrome according to the onset age. Nephrocalcinosis is common in antenatal Bartter syndrome, but is rare in classic Bartter syndrome. It can also be classified into five genetic subtypes by the underlying mutant gene, all of which are expressed in the tubular epithelial cells of the thick ascending limb of the loop of Henle. Patients with Bartter syndrome type 1, 2 and 4 present at a younger age than classic Bartter syndrome type 3. We have experienced a case of Bartter syndrome with nephrocalcinosis in a 42-year-old woman diagnosed by biochemical and radiologic studies. We had successful response with potassium chloride and spironolactone.
The cirrhotic patients with ascites present unique challenge to the renal caregiver. Hydrothorax in a cirrhotic patient treated with PD poses a diagnostic dilemma. Proposed mechanisms for the development of a pleuroperitoneal communication include congenital diaphragmatic defects, acquired weakening of diaphragmatic fibers caused by high intra-abdominal pressures during peritoneal dialysis, and impairments in lymphatic drainage. Pleural fluid analysis and diagnostic imaging assist in differentiation from other causes of pleural effusion. We report a case of hydrothorax in a compensated cirrhotic patient after recent introduction to peritoneal dialysis.
Pheochromocytoma is a catecholamine-producing tumor characterized by hypertension, headache, tachycardia, excessive diaphoresis, and angina pectoris. The thunderclap headache is so named because the pain strikes suddenly and severely. Although the symptoms of bladder pheochromocytoma are rather evident, the diagnosis of this rare neuroendocrine tumor can be missed. This study reports the case of a woman diagnosed with bladder pheochromocytoma who experienced thunderclap headache triggered by urination and angina pectoris as an initial manifestation. This case study suggests that thunderclap headache and angina pectoris occurring concurrently with sudden blood pressure elevation during or immediately after urination are important diagnostic clues of bladder pheochromocytoma.
Citations
Peritonitis is a common and potentially serious infection in patients undergoing continuous ambulatory peritoneal dialysis (CAPD). The most common organisms usually associated with CAPD peritonitis are