Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034186 (pyelonephritis)
 6,144 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The term "renal osteodystrophy" is used to include skeletal disorders of patients with chronic renal failure: osteitis fibrosa, osteomalacia, osteosclerosis, osteoporosis and the frequently associated extraskeletal calcifications. It is the chronic glomerular disease with phosphate retention and resultant hyperphosphatemia on one hand and deficient 1,25 (OH)2 D3 and resultant hypocalcemia on the other to induce secondary hyperparathyroidism. The three most common causes of chronic renal failure in our patients are chronic glomerulonephritis, diabetic nephropathy, hypertensive nephropathy in decreasing frequency, polycystic renal disease occurs in five patients. Other miscellaneous causes include nephrotic syndrome, chronic pyelonephritis, systemic lupus erythematosus, periarteritis nodosa, interstitial nephritis and renal stones. The bone changes are similar in primary and secondary hyperparathyroidism and the incidence of brown tumor is about 3% in the former and 1.5 to 1.7% in the latter. We present one among the 94 dialyzed patients who has long-standing severe chronic renal failure from polycystic kidney disease and develops brown tumor in the mid ulna after 7 years on maintenance hemodialysis. The incidence of brown tumor in our series is about 1.1%. Because of increased longevity of the dialyzed patients, brown tumor from secondary hyperparathyroidism is now more commonly observed. Hyperphosphatemia with serum calcium-phosphate products exceeding plasma solubility of 60 to 75 mg/dl may induce soft tissue and vascular calcification. This explains the much higher incidence of soft tissue calcification in secondary than primary hyperparathyroidism; two of our patients with generalized Monckeberg's type arterial calcification and multiple periarticular calcifications in five patients have been observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal osteodystrophy. 164 77

The clinical and pathological findings are reviewed in ten cases where renal biopsy showed abnormalities predominantly within the interstitium. In six the nephritis was considered to be drug-induced; in two the aetiology was slightly obscure but the most likely diagnosis was considered to be sarcoidosis. Of the remaining two cases one was chronic pyelonephritis and the other polyarteritis nodosa. The diagnosis and pathogenesis of the renal lesions are discussed and attention is drawn to the importance of distinguishing primary interstitial changes from those found in association with glomerular disease.
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PMID:Interstitial nephritis. 725 4

This study focuses on the diagnostic and therapeutic challenge posed by spontaneous perirenal haematomas (SPHs). The medical records of 18 patients with SPHs seen in the past 8 years were reviewed with respect to aetiology, diagnosis and therapeutic management. SPH was secondary to angiomyolipoma (n = 4), polycystic kidneys (n =4), panarteritis nodosa (n = 3), renal cell carcinomas (RCCs, n = 2), glomerulonephritis, pyelonephritis, Morbus Wegener and cortical adenoma (one each). One case remained unclear. With appropriate imaging techniques (computed tomography and angiography) the underlying disorder was detected in 72%; in 4 cases the diagnosis was revealed by exploration and biopsy. Surgery was necessary in 16 patients. The cause of bleeding can be revealed by appropriate imaging in most cases. When imaging procedures fail to reveal the cause of SPH, exploration and biopsy are mandatory to exclude RCC. If the cause of SPH remains unclear even after exploration, patient monitoring by CT is justified.
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PMID:Aetiology, diagnosis and management of spontaneous perirenal haematomas. 874 36

A 54-year-old man was admitted to internal medicine due to unidentified fever persisting for 3 months, and was examined. Then, he was referred to our department for suspected pyelonephritis. Although he was initially being treated for pyelonephritis, right epididymitis occurred during the course of treatment. Antibiotics were ineffective, and symptoms such as weakness and subctaneous nodules also appeared. We performed epididymectomy to differentiate this intractable epididymitis from other systemic diseases. Pathological findings were fibrinoid necrotic vasculitis of middle and small arteries. Of the diagnostic criteria for polyarteritis nodosa, 4 major symptoms and histological findings were satisfied. After we started oral administration of predonin, the fever went down and the creative protein level decreased immediatately.
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PMID:[A Case of Polyarteritis Nodosa Diagnosed from Pathological Findings of Refractory Epididymitis]. 3083 69