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I Koni

Publications and source records attributed to I Koni.

51 records · Page 3Linked to original sources
PubMed1991

Urine anion gap in patients with chronic renal insufficiency.

We investigated the urinary acid excretion and urine anion gap (AG) (Na+ + K(+)-Cl-) during NH4Cl-induced metabolic acidosis in 38 normal subjects and 53 patients with chronic renal diseases in order to clarify the significance of the urine AG as a useful marker of the ammonium (NH4+) excretion even in a state of chronic renal insufficiency. The urine pH became higher, and the urinary excretions of titratable acid (TA) and NH4+ decreased significantly, in parallel with a reduction of the creatinine clearance (Ccr). The urinary electrolyte excretion, especially the chloride excretion, also decreased significantly as Ccr fell. As a result, the urine AG increased from negative to positive values, in proportion to the decrease in Ccr with statistical significance. The urine AG showed the most significant correlation with the urine NH4+ excretion (r = -0.707, p less than 0.001). We conclude that the urine AG provides a significant marker of the urine NH4+ excretion even in a state of moderate to severe renal insufficiency.

Acid-Base Equilibrium↗
PubMed1990

[Bucillamine-associated membranous nephropathy in a patient with rheumatoid arthritis].

A case of bucillamine-associated membranous nephropathy in a patient with rheumatoid arthritis was reported. A 34 year-old woman was admitted to our hospital because of proteinuria in September, 1988. Rheumatoid arthritis had been diagnosed in April, 1988, and had been treated with bucillamine (disease modifying anti rheumatic drug) and amfenac (nonsteroidal antiinflammatory drug). The renal biopsy specimens showed Stage I membranous nephropathy, on both electron and immunofluorescence microscopy. Proteinuria decreased after the drugs were withdrawn despite continued RA symptoms. These results were consistent with drug induced nephropathy. Since bucillamine has some resemblances in its structure and pharmacologic action to D-penicillamine, which sometimes induces membranous nephropathy, it is thought that the nephropathy in this case was caused by an adverse reaction to bucillamine.

Adult↗
PubMed1990

[A case of renal cell carcinoma associated with rapidly progressive glomerulonephritis].

A 74-year-old man was admitted to our hospital because of a treatment for his right renal tumor. The abdominal CT scanning revealed a mass in the right kidney, and a right selective renal arteriography demonstrated a hypervascular tumor. On admission, urinalysis revealed proteinuria (3-4 g/day) and microscopic hematuria, and serum electrolytes were normal. Serum creatinine and urea nitrogen levels were 1.6 mg/dl and 30 mg/dl, respectively. A percutaneous right renal biopsy specimens showed crescentic glomerulonephritis. Direct immunofluorescence studies showed strong linear staining for IgG and IgA along the glomerular capillary walls. Electron microscopy showed increased mesangial matrix and swollen epithelial cells, but no dense deposits in the para-mesangial area and in the glomerular basement membrane. The patient underwent right radical nephrectomy. Histologic examination of the resected specimen revealed renal cell carcinoma. Postoperatively, he developed rapidly progressive renal failure and the renal function could not be recovered. Using the indirect immunofluorescence technique, we could not confirm the presence of a serum anti-glomerular basement membrane antibody, although the examination could not be carried out until the initiation of hemodialysis therapy. Some cases of glomerulopathies associated with renal cell carcinoma were previously reported, but the case of crescentic glomerulonephritis was very rare.

Aged↗