occupational renal diseases by: dr. majid golabadi
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Occupational Renal Diseases
By: Dr. Majid Golabadi
Introduction The etiology of the renal failure in a significant
percentage of patients is never fully elucidated
Diagnosis of renal disease of occupational origin is rarely considered.
The true incidence of chronic kidney disease secondary to occupational and environmental exposures is unknown.
These exposures represent potentially preventable causes of chronic kidney disease.
The kidney is especially vulnerable to occupational and environmental exposures.
Occupational and environmental toxins can be highly concentrated in the kidney
Monitoring workers for the possible renal effects of occupational exposures is very difficult: lack of sensitive and specific tests of renal injury Serial measurement of the traditional tests such as
creatinine or blood urea nitrogen (BUN) is inadequate
The currently recommended tests: possible glomerular injury (urine albumin) proximal tubule damage (retinol binding protein, N-
acetyl-β-D-glucosaminidase, alanine amino peptidase) distal tubule injury (osmolality)
ACUTE RENAL DYSFUNCTION A large number of occupational and environmental toxins can
cause acute renal failure, usually after high-dose exposure Most common: acute tubular necrosis (ATN) Hours to days after the exposure
Manifestations: decreased urine output (oliguric range of less than 500 mL/d). renal tubular cells, granular casts, and little or no protein. Without Red blood cells, white blood cells, or casts Increases in BUN and creatinine Recovery: after 1-2 weeks, with diuresis
Occupational causes of ARF 1. heavy metals:
Significant exposure to any of the divalent metals (chromium, cadmium, mercury, and vanadium)
Welders exposed to cadmium fumes Severe exposure: bilateral cortical necrosis
2. Organic solvents Halogenated hydrocarbons Nonhalogenated hydrocarbons
Halogenated hydrocarbons
Carbon tetrachloride (CCl4)Acute abdomen, 7-10 days, prerenal azotemia
Ethylene dichloride (C2H4CI2) Chloroform (CCI3H) TetrachloroethaneThe most toxic Vinylidene chloride
Nonhalogenated hydrocarbons
Dioxane acute abdomen Toluene Glu sniffing, metabolic acidosis Alkyl derivatives of ethylene glycol Phenol Local burns, Albuminuria, RBC, hypothermia
and convulsion, carboluria
Nonhalogenated hydrocarbons PentachlorophenolSkin, hypermetabolic state, hyperpyrexia Dinitriphenols Fatal hyperpyrexia
ARF caused by unidentified pesticides
Reduction in GFR Tubular reabsorption of phosphate organophosphate
Occupational causes of ARF Arsine (AsH3) is a heavy gas and is the
most nephrotoxic form of arsenic. Exposures: semiconductor industry a potent hemolytic agent Renal failure due to hemoglobinuria.
elemental yellow phosphorus: acute hepatic and acute renal necrosis Chronic exposure: proteinuria
Balkan-Endemic Nephropathy
Interstitial nephritis Aristolochic acid Papillary transitional cell cancer
Analgesic nephropathy Renal dysfunction as a consequence of NSAIDs
and cyclooxygenase inhibitors three different forms:
hemodynamic renal failure (loss of prostaglandin-mediated afferent arteriolar vasodilation)
acute renal failure secondary to acute interstitial nephritis (accompanied by nephrotic range proteinuria)
Both forms: reversible after discontinuation of the offending drug
papillary necrosis (not reversible): occurs after many years of high doses of NSAIDs.
It is controversial whether chronic acetaminophen use causes papillary necrosis.
CHRONIC KIDNEY DISEASE
Most common causes:
Lead
Cadmium
Mercury
Silica
Organic solvents
Chronic renal dysfunction
Interstitial tubular nephritis
1-Heavy metals• (lead, cadmium)
2-Pesticides
Nephrotic syndrome
1-Organic solvents 2-Silicosis 3-Mercury
Lead Occupations:
battery-making, smelting, painting, glazing, mining
Accumulates in the body (mainly in bones)
The classic presentation: history of hypertension and gout 1+ to 2+ proteinuria without cells or cellular casts or
normal 24h urine collection: nonnephrotic range proteinuria renal ultrasonography: small, contracted kidneys. Renal biopsy: nonspecific tubular atrophy, interstitial
fibrosis, and minimal inflammatory infiltrates Inclusion body
Diagnosis: documenting significant lead exposure Serum lead levels are not useful unless
elevated, because low serum levels do not exclude chronic lead exposure.
Treatment: Continued EDTA injections thrice weekly, with the
goal of normalizing the urinary lead chelate. The oral lead chelator DMSA is currently being
studied
Cadmium Occupations: welding, battery-making, smelting,
mining, soldering, pigment-producing, plating
accumulates in the body having a biological half-life in humans in excess of 10 years (40% to 80% in the liver and kidneys)
Fanconi syndrome, Hypercalciuria with normocalcemia, hyperphosphaturia, and distal renal tubular acidosis all contribute to the osteomalacia, pseudofractures, and nephrolithiasis
PTH
Mercury Occupations: medical equipment, environmental
exposure
accumulates in the proximal tubule
acute tubular necrosis and nephrotic syndrome
Membranous nephropathy, minimal change disease,
Treatment: removal from exposure and chelation with British antilewisite (dimercaprol BAL).
Beryllium
Granulomas, interstitial fibrosis Hypercalciuria, renal stone PTH hyperuricemia
Silica Silicosis is a form of pneumoconiosis
associated with pulmonary exposure to silica.
Heavy exposure: generalized systemic
disease
Glomerulonephritis with immune mechanism
Organic solvents Solvent exposure may occur in many
industries where there is use of paints, degreasers, and fuels, including the petrochemical and aerospace industries.
antiglomerular basement membrane antibody-mediated glomerulonephritis
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