Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sera from 35 patients with biopsy-proven diffuse proliferative (WHO class IV) or membranous (WHO class V) lupus nephritis were analyzed for the presence and size of circulating immune complexes. Elevations of the C1q solid-phase assay (C1qSP) for immune complexes were found in sera from all patients with diffuse proliferative nephritis, with a mean +/- 1 SEM of 166.8 +/- 42.0 micrograms/AHG-equivalents/ml serum, and in 71.4% of the patients with membranous nephritis (83.1 +/- 26.7, p = 0.06). Using the WHO criteria for subclasses of membranous lupus nephritis, we also designated renal biopsies as nonproliferative (WHO classes Va and Vb) or proliferative (WHO classes IV and Vc). Employing the latter groupings, we observed significant differences between C1qSP results of patients with nonproliferative (30.3 +/- 8.8) and proliferative (172.8 +/- 36.8, p less than 0.001) lupus nephritis. These data suggest that the presence of C1q-binding material in serum is pathophysiologically related to proliferative glomerular lesions, and that levels of C1qSP binding reflect renal lesions in SLE patients. Sucrose density gradient ultracentrifugation was performed on each serum, and gradient fractions analyzed for C1qSP-binding and total IgG, using techniques to minimize losses of immune complexes. The predominant peak of C1qSP activity sedimented with the 6.6S monomeric IgG. The 6.6S C1q-binding IgG was increased only in 1 of 10 patients with membranous lupus nephritis without proliferative changes, and was elevated in 16 of 25 patients with proliferative lesions (WHO classes IV and Vc). A significant negative correlation was found between the presence of this C1q-binding material and subepithelial electron-dense deposits, suggesting that the presence of this material contributed to the absence of subepithelial immune deposits. Large-molecular-weight C1qSP-binding material was also present, mainly in sera from patients with proliferative lesions. Furthermore, highly positive correlations were found between immune deposits in interstitial blood vessels and peritubular areas, and the concentrations of C1qSP-binding IgG and rapidly sedimenting IgG in density gradient analysis. Overall, these findings are consistent with the hypotheses that circulating immune complexes contribute to the pathogenesis of glomerulonephritis and interstitial nephritis in patients with SLE, and that 6.6S C1q-binding IgG plays a role in the proliferative lesions of lupus glomerulonephritis.
 ...
PMID:Relationship between renal pathology and the size of circulating immune complexes in patients with systemic lupus erythematosus. 310 94

Ca metabolism was compared in two groups of patients with chronic interstitial nephritis: in 21 patients (analgesic abuse nephropathy (AAN) group), nephropathy was due to exposure for 5-50 years (mean 21.1) to phenacetin-containing analgesics, whereas in 21 other patients (controls) it was due to exposure for 1-80 years (mean 21.4; NS) to other causes. Patients were followed for 2.5 +/- 0.6 and 1.6 +/- 0.6 years, respectively (mean +/- SEM; NS). Blood Ca, P, protein, creatinine, alkaline phosphatase, parathyroid hormone (PTH), 25-hydroxyvitamin D (25(OH)D), 1,25-dihydroxyvitamin D (1,25(OH)2D) as well as arterial acid-base status and urinary excretion rate of Ca, P and creatinine were determined serially. Results were included only when P was maintained between 0.7 and 1.9 mmol/l. The range of creatinine levels studied was 95-1,600 mumol/l. No differences were found between the two groups with respect to creatinine clearance, blood P, protein, arterial pH and bicarbonate, and urinary excretion rates of Ca and P. Mean plasma Ca was significantly lower, and PTH was significantly higher in the AAN group than in the control group; mean plasma alkaline phosphatase activity was also significantly higher in the AAN group. In both groups Ca was negatively correlated with creatinine, but the slope of the regression line was steeper in the AAN group than in controls. The degree of hypocalcemia was related to the increase in plasma PTH and alkaline phosphatase, but not to the plasma level of 25(OH)D or 1,25(OH)2D.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Evidence for a particularly severe secondary hyperparathyroidism in analgesic abuse nephropathy. 406 3

Mononuclear inflammatory cells (MIC) in renal biopsies from 37 patients with renal disease were studied by avidin--biotin--immunoperoxidase complex (ABC) technique, utilizing monoclonal antibodies to cell surface antigens: T11 (total T), T4 (inducer/helper), T8 (suppressor/cytotoxic), B1 (B cells), M1 (monocytes), and Leu-7 (natural killer, NK cells). Renal MIC consisted mostly of T cells and monocytes. T cells were a predominating cell type in the renal interstitium of all patients studied (64-88% of MIC). The T4:T8 ratios ranged from 0.4 +/- 0.3 (mean +/- SEM) in interstitial nephritis to 2.5 +/- 0.9 in membranous glomerulonephritis. M1+ cells constituted from 10 to 62% of glomerular MIC and from 5 to 24% of interstitial MIC. Glomerular MIC were rare or absent in patients with IgA nephropathy (IgA N). These results support the concept that in situ interactions of T lymphocytes and monocytes may modulate the events leading to the development of human renal disease. The striking absence of glomerular MIC in IgA N could be related to persistence of immune deposits in the glomeruli of patients with this renal disorder.
 ...
PMID:Mononuclear cell subsets in human renal disease. Enumeration in tissue sections with monoclonal antibodies. 660 1

Calcium (Ca) metabolism was compared in 2 groups of patients with chronic interstitial nephritis: in 21 patients (AAN-group) nephropathy was due to exposure for 5 to 50 years (mean 21.1) to phenacetin containing analgesics, whereas in 21 other patients (controls) it was due to exposure for 1 to 80 years (mean 21.4) (NS) to other causes. Patients were followed for 2.5 +/- 0.6 and 1.6 +/- 0.6 years respectively (mean +/- SEM) (NS). Blood Ca, P, protein, creatinine, alkaline phosphatase, parathyroid hormone (PTH), 25-hydroxyvitamin D (25-OH-D), together with arterial acid-base status and urinary excretion rate of Ca, P and creatinine were measured serially. For each patient the results were averaged for 2 degrees of renal failure, i.e. for creatinine levels below and above 400 mumol/l (logarithmic mean). Results were included only when P was maintained between 0.7 and 1.9 mmol/l. The range of creatinine levels studied was 95 to 1600 mumol/l. No differences were found between the 2 groups with respect to creatinine clearance, blood, P, protein, arterial pH and urinary excretion rates of Ca and P. There was a trend for blood HCO3 to be lower in the AAN group. Mean plasma Ca was significantly lower, and PTH was significantly higher, in the AAN than in the control group at both degrees of renal failure; mean plasma alkaline phosphatase activity was also significantly higher in the AAN group, but at severe degrees of renal failure only. Significant correlations were observed between individual values of both Ca and PTH (r = -0.747) and PTH and alkaline phosphatase (r = 0.603). The degree of hypocalcemia and of hyperparathyroidism was not related to the plasma level of 25-OH-D. It is concluded that at comparable degrees and duration of renal failure patients with AAN, when compared with patients with interstitial nephritis of other origins, have lower blood Ca and consequently higher PTH levels and alkaline phosphatase activities, suggesting more severe osteodystrophy.
 ...
PMID:[Particularly severe calcium metabolic disorder in nephropathy from analgesic abuse]. 717 76

The Ramipril Efficacy in Nephropathy (REIN) study found that angiotensin-converting enzyme (ACE) inhibitors effectively decreased proteinuria, glomerular filtration rate (GFR) decline (DeltaGFR), and incidence of end-stage renal disease (ESRD) in patients with proteinuric chronic nephropathies. In this study, we prospectively investigated the main clinical determinants of progression and response to treatment in the 352 patients enrolled into the REIN study. Mean DeltaGFR (0.56 +/- 0.05 [SEM] versus 0.21 +/- 0.05 mL/min/1.73 m(2)/mo; P = 0.0001) and incidence of ESRD (30% and 10%; P = 0.0001) were more than twice that in patients with proteinuria of 2 g/24 h or greater of protein compared with those with protein less than 2 g/24 h (relative risk [RR], 4.07; 95% confidence interval [CI], 2.20 to 7.52), as well as in patients with hypertension compared with normotension (mean DeltaGFR, 0.48 +/- 0. 05 versus 0.22 +/- 0.05 mL/min/1.73 m(2)/mon; P = 0.0006; ESRD, 25% versus 10%; P = 0.004; RR, 3.18; 95% CI, 1.38 to 7.32). Hypertension at study entry (P = 0.038), greater mean blood pressure on follow-up (P = 0.002), and urinary protein excretion rate (P = 0.0001) were independent predictors of faster DeltaGFR. DeltaGFR was approximately twofold faster in patients with type 2 diabetes than in those with primary glomerular disease (P = 0.002; including immunoglobulin A [IgA] nephropathy, P = 0.009); nephrosclerosis (P = 0.03), adult polycystic kidney disease (APKD), or chronic interstitial nephritis (P = 0.006). Diabetes at study entry (P = 0. 02) and greater mean blood pressure (P = 0.0001) and urinary protein excretion rate (P = 0.0001) on follow-up were independent predictors of faster DeltaGFR. After correction for baseline covariates, diabetes was also associated with an increased risk for progression to ESRD (RR, 2.39; 95% CI, 1.01 to 5.68; P < 0.05). At multivariate analyses, ramipril significantly decreased DeltaGFR (regression coefficient,-0.23 +/- 0.11 [SEM]; P = 0.036) and ESRD (RR, 2.08; 95% CI, 1.21 to 3.57; P = 0.008) in patients with baseline proteinuria of 2 g/24 h or greater of protein, and the renoprotective effect increased for increasing levels of proteinuria. Ramipril decreased DeltaGFR to a similar extent in normotensive and hypertensive patients (-0.14 +/- 0.11 versus -0.14 +/- 0.09) and significantly limited ESRD in hypertensive patients (RR, 2.03; 95% CI, 1.26 to 3. 26; P = 0.004). DeltaGFR was decreased by 42% in primary glomerular disease (P = 0.017), by 35% in IgA nephropathy, and by 37% in nephrosclerosis, but was not improved in type 2 diabetes, APKD, or interstitial nephritis. At multivariate analyses, ramipril significantly slowed DeltaGFR (-0.24 +/-0.08; P = 0.004) and progression to ESRD (RR, 2.32; 95% CI, 1.36 to 3.96; P = 0.002) in patients without diabetes, but not in patients with diabetes, who tended to have a faster DeltaGFR (+0.62 +/- 0.44) on ramipril therapy. In summary, patients with proteinuria of 2 g/24 h or greater of protein, preexisting hypertension, or type 2 diabetes were faster progressors. Greater blood pressure and degree of proteinuria were the strongest determinants of faster GFR decline. The renoprotective effect of ramipril was similar in patients with normotension and hypertension. Hypertensive patients and those with proteinuria of 2 g/24 h or greater of protein, primary glomerular disease, or nephrosclerosis gained the most from ACE inhibitor treatment. During the study period, those with proteinuria less than 2 g/24 h of protein, type 2 diabetes, or polycystic kidney disease did not benefit by treatment to an appreciable extent.
 ...
PMID:Chronic proteinuric nephropathies: outcomes and response to treatment in a prospective cohort of 352 patients with different patterns of renal injury. 1084 31

The histomorphologic characteristics and chemical composition of the crystals associated with suspected pet food-induced nephrotoxicosis in 3 dogs are described. Kidney specimens from 2 dogs, a 3-year-old Parson Russell Terrier and a 3-year-old Bernese Mountain Dog, were examined. Both developed acute renal failure after eating canned pet food on the 2007 Menu Foods recall list. The third case was a kidney specimen from a 1-year-old mixed-breed dog from a similar 2004 outbreak of canine renal failure in Taiwan, which occurred after eating a commercial dog food. Hematoxylin and eosin (HE), 72-hour Oil Red O (ORO72h), Alizarin Red S (pH 4.1-4.3), and Von Kossa stains; infrared (IR) spectroscopy; and scanning electron microscopy with energy dispersive X-ray analysis (SEM/EDXA) were performed to determine the histomorphologic characteristics and chemical composition of the crystals observed in each case. Histomorphologic findings in each case included acute, marked tubular degeneration and necrosis with many intratubular birefringent crystals, and lymphoplasmacytic interstitial nephritis. In each case, most of the crystals were rough, pale brown, and stained with ORO72h but did not stain with Alizarin Red S (pH 4.1-4.3) or Von Kossa stains; these features were consistent with a plastic or lipid. IR spectroscopy and SEM/EDXA results were consistent with melamine-containing crystals. A second crystal type identified in each case was smooth and platelike with staining characteristics and IR spectroscopy and SEM/EDXA results consistent with calcium oxalate crystals. Melamine-containing crystals have distinct light microscopic, histochemical, and SEM/EDXA characteristics that facilitate their identification in tissue.
 ...
PMID:Characterization of melamine-containing and calcium oxalate crystals in three dogs with suspected pet food-induced nephrotoxicosis. 1848 5