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Nephropathy

The alimentary symptoms may be overshadowed by neuromuscular dysfunction, accompanied by signs of motor weakness that may progress to paralysis of the exterior muscles or the wrist (wrist drop), and less often, of the ankles (foot drop). Encephalopathy, the most serious result of lead poisoning, frequendy occurs in children as a result of pica, ie, ingestion of inorganic lead compounds in paint chips this rarely occurs in adults. Nephropathy has also been associated with chronic lead poisoning (147). The toxic effects of lead may be most pronounced on the developing fetus. Consequendy, women must be particulady cautious of lead exposure (148). The U.S. Center for Disease Control recommends a blood level of less than 10 p.m per 100 mL for children. [Pg.73]

Lead is toxic to the kidney, cardiovascular system, developiag red blood cells, and the nervous system. The toxicity of lead to the kidney is manifested by chronic nephropathy and appears to result from long-term, relatively high dose exposure to lead. It appears that the toxicity of lead to the kidney results from effects on the cells lining the proximal tubules. Lead inhibits the metaboHc activation of vitamin D in these cells, and induces the formation of dense lead—protein complexes, causing a progressive destmction of the proximal tubules (13). Lead has been impHcated in causing hypertension as a result of a direct action on vascular smooth muscle as well as the toxic effects on the kidneys (12,13). [Pg.78]

In some patients with IgA nephropathy (IgAN), intraglomerular coagulation plays a role in depositing fibrinogen (235,236). IgAN patients treated with urokinase show a marked improvement in urinary protein concentration, semm creatinine, and blood urea nitrogen levels (237). [Pg.312]

Encephalopathic signs and Chronic nephropathy Colic, other overt ... [Pg.370]

In the treatment of hypertension, ACE inhibitors are as effective as diuretics, (3-adrenoceptor antagonists, or calcium channel blockers in lowering blood pressure. However, increased survival rates have only been demonstrated for diuretics and (3-adrenoceptor antagonists. ACE inhibitors are approved for monotherapy as well as for combinational regimes. ACE inhibitors are the dtugs of choice for the treatment of hypertension with renal diseases, particularly diabetic nephropathy, because they prevent the progression of renal failure and improve proteinuria more efficiently than the other diugs. [Pg.10]

Increased mortality was observed in both male rats (at doses of 20.4 mg/kg/day and above) and male mice (at doses of 0.46 mg/kg/day and above) in a 2-year bioassay conducted by the National Cancer Institute (NCI 1978). The authors attributed the excessive mortality in the male rats to treatment-related toxic nephropathy. The high mortality in male mice was possibly due to fighting since no other treatment-related cause for the deaths could be determined. Survival in females of both species was unaffected by endosulfan (NCI 1978). However, survival was significantly decreased in female rats that consumed 5 mg/kg/day for 2 years (FMC 1959b), and in female mice that consumed approximately 2.9 mg technical endosulfan/kg/day for 2 years (Hack et al. 1995 Hoechst 1988b). In these studies, survival in male rats was not affected at 5 mg/kg/day for 2 years (FMC 1959b) and survival in male mice was not affected at 2.51 mg/kg/day for 2 years (Hoechst 1988b). [Pg.49]

Lameier NH. Contrast-induced nephropathy—prevention and risk reduction. Nephrol... [Pg.31]

Other electrolytes of importance include calcium (especially if the patient is receiving a calcium channel blocker, such as nicardipine) and magnesium, as hypomagnesemia may predispose the patient to seizures, further complicating the ICP management. If the patient received intravenous iodinated contrast as part of their stroke evaluation, then careful monitoring of the blood urea nitrogen (BUN) and creatinine levels is necessary to detect contrast nephropathy. [Pg.166]

Prevention of diabetic complications such as retinopathy, nephropathy, cardiomiopathy. [Pg.355]

In order to identify chemically the so-caUed monascidin A discussed by some Chinese scientists in their papers as a component suitable for the preservation of food, it was isolated and chemical investigations using mass spectrometry and NMR were undertaken. Monascidin A was characterized as citrinin which is known to be a mycotoxin responsible for nephropathies. Thus, in order to avoid the production of this toxin, various strains were screened in order to see whether all were toxino-genic and it was shown that among the species of Monascus available in pubhc collections, non-toxinogenic strains were obtainable. [Pg.416]

Diabetes continues to be a major cause of excessive morbidity, severe disability and premature death in Western populations. In developed countries, the cost of diabetes to society may be estimated to be as high as 5% of the total health costs, much of which relates to the chronic vascular complications of this disorder (Williams, 1991). The vascular lesion in diabetes consists of (1) microangiopathy, distinguished by thickening of capillary basement membranes resulting in increased vascular permeability, which is clinically manifested as diabetic retinopathy (Fig. 12.1a) and/or nephropathy (Fig. 12.1b), and (2) macroangiopathy (Fig. 12.2),... [Pg.183]

Figure 12.1 (a) Diabetic microangiopathy pre-proliferative retinopathy, (b) Diabetic microangiopathy glomerular disruption and degeneration In diabetic nephropathy. [Pg.184]

A volume >5 mL/kg divided by serum creatinine in mg/dL associated with increased risk of nephropathy... [Pg.156]

Diabetic or HIV nephropathy, analgesic abuse nephropathy, cyclosporine nephropathy, and chronic interstitial nephritis... [Pg.178]

Chymostatin-sensitive Il-generating enzyme Carvedilol Post-Infarct Survival Control in Left Ventricular Dysfunction Trial Collaborative Study Captopril Trial ( The Effect of Angiotensin-Converting Enzyme Inhibition on Diabetic Nephropathy ) calcium channel blocking agents Candesartan in Heart Failure Assessment of Reduction in Morbidity and Mortality Trial congestive heart failure, but the latest recommendations use HF for heart failure chronic kidney disease cardiac output... [Pg.31]


See other pages where Nephropathy is mentioned: [Pg.665]    [Pg.338]    [Pg.338]    [Pg.490]    [Pg.498]    [Pg.498]    [Pg.49]    [Pg.369]    [Pg.124]    [Pg.275]    [Pg.431]    [Pg.480]    [Pg.494]    [Pg.400]    [Pg.400]    [Pg.762]    [Pg.2158]    [Pg.88]    [Pg.11]    [Pg.13]    [Pg.90]    [Pg.148]    [Pg.202]    [Pg.196]    [Pg.155]    [Pg.160]    [Pg.169]    [Pg.221]    [Pg.20]    [Pg.25]   
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Acetaminophen analgesic nephropathy

Acute phosphate nephropathy

Acute uric acid nephropathy

Aminoaciduria lead nephropathy

Analgesic nephropathy

Analgesic nephropathy Australia

Analgesic nephropathy Belgium

Analgesic nephropathy United States

Analgesic nephropathy analgesics

Analgesic nephropathy caffeine + aspirin

Analgesic nephropathy diagnosis

Analgesic nephropathy different analgesics

Analgesic nephropathy epidemiology

Analgesic nephropathy papillary calcifications

Analgesic nephropathy phenacetin

Analgesic nephropathy prevention

Analgesic nephropathy renal imaging

Anemia Balkan nephropathy

Anemia lead nephropathy

Angiotensin-converting enzyme diabetic nephropathy

Angiotensin-converting enzyme inhibitors diabetic nephropathy treatment

Apoptosis Balkan nephropathy

Aristolochic acid nephropathy

Aristolochic acid nephropathy Aristolochia

Aristolochic acid nephropathy Japan

Aspirin analgesic nephropathy

Balkan endemic nephropathy

Balkan nephropathy

Balkan nephropathy animals

Balkan nephropathy cadmium

Balkan nephropathy chromosomes

Balkan nephropathy cyclosporine

Balkan nephropathy diagnosis

Balkan nephropathy environment

Balkan nephropathy epidemiology

Balkan nephropathy etiology

Balkan nephropathy exposure

Balkan nephropathy genetic factors

Balkan nephropathy genetics

Balkan nephropathy immunology

Balkan nephropathy incidence

Balkan nephropathy prevalence

Balkan nephropathy treatment

Balkan nephropathy viruses

Balkan nephropathy water

Balkan nephropathy wells

Bulgaria Balkan nephropathy

Cadmium nephropathy

Caffeine analgesic nephropathy

Calcium lead nephropathy

Captopril diabetic nephropathy treatment

Carcinoma Balkan nephropathy

Carcinoma analgesic nephropathy

Carcinoma aristolochic acid nephropathy

Cast nephropathy

Chelation therapy lead nephropathy

Chinese herb nephropathy

Chronic allograft nephropathy

Chronic progressive nephropathy

Chronic progressive nephropathy associated with

Chronic progressive nephropathy incidence

Citrinin Balkan nephropathy

Codeine analgesic nephropathy

Contrast media-induced nephropathy

Contrast-induced nephropathy pathogenesis

Contrast-induced nephropathy prevention

Contrast-induced nephropathy risk factors

Crystal nephropathy

Diabetes mellitus nephropathy

Diabetic nephropathy management

Diabetic nephropathy risk factors

Diabetic nephropathy urine albumin

Drug-related nephropathies

Encephalopathy lead nephropathy

Environmental exposure lead nephropathy

Fanconi syndrome lead nephropathy

Fetal reflux nephropathy

Glomerular nephropathy

Glycosuria lead nephropathy

Gouty nephropathy

Hemodialysis Balkan nephropathy

Heroin nephropathy

Hyaline droplet nephropathy

Hypertension hypertensive nephropathy

Hypertension lead nephropathy

Hypertensive nephropathy

Hyperuricemia lead nephropathy

Hyperuricemic nephropathy

Idiopathic membranous nephropathy

IgA nephropathy

Immune nephropathies

Immune response nephropathies

Immunoglobulin A nephropathy

In immunoglobulin A nephropathy

In membranous nephropathy

In minimal-change nephropathy

Inclusion bodies lead nephropathy

Interstitial fibrosis lead nephropathy

Interstitial nephritis lead nephropathy

Kidney disease diabetic nephropathy

Kidney disease hypertensive nephropathy

Kidney disease toxic nephropathy

Kidney nephropathy)

Lead nephropathy

Lead nephropathy Queensland

Lead nephropathy absorption

Lead nephropathy acute

Lead nephropathy chronic

Lead nephropathy experimental

Lead nephropathy exposure

Lead nephropathy occupational

Lead nephropathy toxicity

Lead nephropathy treatment

Membranous nephropathy

Membranous nephropathy corticosteroids

Membranous nephropathy drug-induced

Membranous nephropathy treatment

Microalbuminuria hypertensive nephropathy

Minimal-change nephropathy

Minimal-change nephropathy proteinuria

Minimal-change nephropathy treatment

Mycotoxins Balkan nephropathy

Nephropathy contrast-induced

Nephropathy drug-induced

Nephropathy immunoglobulin

Nephropathy obstructive

Nephropathy prevention

Nephropathy sickle cell

Nephropathy toxic

Nephropathy urine albumin

Nephropathy, chronic

Nephropathy, diabetic

Occupational exposure lead nephropathy

Ochratoxin Balkan nephropathy

Parenchymal nephropathy

Phosphates nephropathy

Progressive irreversible nephropathy

Prostaglandins analgesic nephropathy

Proteinuria Balkan nephropathy

Proteinuria in membranous nephropathy

Radiation nephropathy

Reflux nephropathy

Relevance of Rat a2u-Globulin Nephropathy and CPN to Humans

Renal calcification analgesic nephropathy

Renal disease diabetic nephropathy

Renal disease hypertensive nephropathy

Renal disease toxic nephropathy

Renal function impairment nephropathy

Renal papillary necrosis analgesic nephropathy

Role of the Maillard Reaction in Nephropathy

Romania Balkan nephropathy

Salicylate analgesic nephropathy

Serbia Balkan nephropathy

Symptoms of Nephropathy

Transplantation chronic allograft nephropathy

Tubular atrophy lead nephropathy

Tubulointerstitial nephropathy

Urate nephropathy, chronic

Uric acid nephropathy

Urothelial tumors Balkan nephropathy

Vitamin lead nephropathy

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