Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 63-year-old woman who had received hemodialysis therapy since she fell acute on chronic renal failure 4 years ago presented with multiple joint pain. Nephrocalcinosis was not detected by abdominal X-ray when hemodialysis therapy was initiated. Laboratory testing showed azotemia, anemia, hypoproteinemia and mild liver dysfunction but no liver cirrhosis. Biopsied bone tissue demonstrated numerous calcium oxalate crystal depositions. Laparoscopy revealed black liver in macroscopic view. Histological studies showed numerous lipofuscin-like dark brown granules were deposited in hepatocytes. The activity of alanine : glyoxylate aminotransferase (AGT) was less than 0.1 U/g in biopsied patient's liver tissue. Generally, clinical symptoms demonstrated by Japanese primary hyperoxaluria type I (PH-I) patients are milder than those of European patients. Some PH-I patients may successfully avoid urinary tract calcification unless they fall into oliguria by some other causes. The lipofuscin granules are most likely the source of the dark color. Massive deposition of the lipofuscin granules indicated that the duration of the liver metabolic abnormality had lasted for long time. Thus, black liver may be related to a mild form of PH-I.
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PMID:A case of late onset primary hyperoxaluria type I (PH-I) presented with black liver. 977 23

Sonographic findings of renal medullary hyperechogenicity have been observed in the neonate in association with severe perinatal renal injury, kidney malformations or nephrocalcinosis, and, rarely, in newborn infants with transient renal failure. The aim of the study was to describe the entity of neonatal transient renal failure with renal medullary hyperechogenicity (NTRFMH). We studied nine term neonates, born between August 1999 and February 2004 in our institution (0.1% of the live born infants), who developed transient renal dysfunction after birth, and in whom renal sonograms showed bilateral medullary hyperechogenicity. Seven of the infants (78%) had anuria until 30-45 hours of age, and two (22%) had oliguria. Peak serum creatinine levels ranged between 0.61 and 1.62 mg/dL (mean: 1.09+/-0.27 mg/dL) at 2-3 days of life. Additional findings included proteinuria in nine infants (100%), uric acid crystalluria in seven (78%), hyperuricemia in four (44%), and hypertension in one (11%). Hyperuricosuria was demonstrated in one out of the seven patients in whom this parameter was determined. Urinary excretion rates of calcium, phosphorus and oxalic acid were normal, as were urinary levels of amino acids and organic acids. Full clinical recovery accompanied by normalization of all laboratory parameters was observed in all infants by 4-6 days of life. Subsequent follow-up showed normal renal function, no urinary abnormalities, and normal renal sonograms in all infants. Our summary of the nine infants with NTRFMH reported on here and a review of 19 cases of this condition reported in the literature reveal a not-so-rare entity of unclear etiology, but excellent prognosis. Physicians caring for neonates should be aware of this benign and transient condition.
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PMID:Neonatal transient renal failure with renal medullary hyperechogenicity: clinical and laboratory features. 1588 Feb 71