Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0026764 (
multiple myeloma
)
36,148
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Hypercalcemia is frequently observed in patients with
multiple myeloma
and renal failure. Whether Bence Jones protein (BJP) is directly nephrotoxic and how and whether hypercalcemia might contribute to this putative nephrotoxicity is currently unclear. To examine this issue, we studied the effect of modest hypercalcemia on the glomerular filtration rate (GFR) of rats exposed to a BJP that by itself had been found to be nonnephrotoxic. Three groups of rats were studied. All were anesthetized and underwent a baseline measurement of inulin clearance (Cin). After this, group 1 (n = 13) rats were given 2 ml of vehicle (phosphate-buffered saline solution [PBS]) and were then made hypercalcemic with an infusion containing 0.048 mol/L
CaCl2
. At the end of 2 hours a second Cin was measured. Group 2 rats (n = 8) were given 100 mg BJP in 2 ml PBS and a non-calcium-containing infusate. Group 3 (n = 11) rats were given 100 mg of the BJP in 2 ml PBS and then the calcium-containing infusate used in group 1 rats. Rats in groups 2 and 3 also had a second Cin measured at the end of 2 hours. Renal blood flow was measured with an electromagnetic flow probe. At the completion of the second clearance, kidneys were processed for renal histologic assessment. The serum calcium level measured during the second Cin period was 13.5 mg/dl for group 1, 7.9 mg/dl for group 2, and 13.7 mg/dl for group 3. No significant decrement in GFR was observed in group 1 or 2 rats. In contrast, group 3 rats had a 46% fall in GFR.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Hypercalcemia can potentiate the nephrotoxicity of Bence Jones proteins. 365 25
Circulating antibody to Tamm-Horstall protein (THP) was measured using a radioimmunoassay in forty-five patients on maintenance hemodialysis and compared to levels of antibody titers measured in sera from ten healthy controls. The etiology of the end-stage kidney disease in the patient population was polycystic kidney disease in thirteen, glomerulonephritis in fourteen, diabetic nephropathy in nine, interstial nephritis and chronic pyelonephritis in three each,
multiple myeloma
in two, and urinary tract obstruction in one. Four patients had significantly elevated titers of antibody to THP but shared no other unifying characteristics. The results also indicate that none of the groups studied had mean antibody titers significantly different from controls. Furthermore, no general trend was apparent between levels of antibody to THP and number of months on dialysis. Observations made during the study revealed that heparinized samples of blood had lower titers of antibody to THP than did non-heparinized samples from the same patient. This finding was repeated when other anti-coagulants, i.e., ethylenediaminetetraacetate (EDTA) and sodium citrate, were used. Titers returned toward normal when
CaCl2
was added back to samples anticoagulated with EDTA and sodium citrate. This suggests that clotting factors, probably fibrinogen, interfered with the measurement of antibody titers. Therefore, only serum should be used in further investigations of THP antibody using this assay.
...
PMID:Tamm-Horsfall protein antibody in patients with end-stage kidney disease. 739 72