Renal Urinary protein

Polyalphaolefin Hydraulic Fluids. The only information on renal effects in humans or animals following inhalation, oral, or dermal exposure to polyalphaolefin hydraulic fluids is a report of increased urinary protein to creatinine ratio of rats orally exposed to MIL-H-83282 at 1,000 mg/kg/day for 4 weeks. Diuresis was noted in rats similarly exposed to MIL-H-83282LT (Mattie et al. 1993). 

Male rats are sensitive to renal tubular nephropathy after exposure to hexachloroethane. The lesions observed are characteristic of hyaline droplet nephropathy. They are most likely the result of hexachloroethane or one of its metabolites binding to the excretory protein 2p-globulin, altering its kidney transport, and leading to the formation of hyaline droplets. This protein is synthesized by male rats and accounts for 26% of their urinary protein excretion (Olson et al. 1990). It is not excreted in female rats except in minimal quantities. Since some effects are also seen in kidneys of female rats and in male and female mice that do not synthesize 2p-globulin, hexachloroethane must also have milder adverse effects on the kidney through a different mechanism. 

The urine frequently contains casts and amorphous debris, but rarely any considerable number of red blood corpuscles. Proteinuria and aminoaciduria are found in nearly all untreated patients from a very early age. The proteinuria is usually reported as albuminuria in the literature, but in some cases the urinary protein has been shown by electrophoresis to consist largely of a-globulin and other relatively low-molecular-weight proteins (B21). A similar urinary pattern occurs in a number of diseases of the renal tubule. The proteinuria is often only moderate in degree, e.g., < 50 to 150 mg protein per 100 ml of urine, but is easily detected by the conventional tests for protein, such as salicylsulfonic acid. Excretion of protein can rise to nearly 1 g/100 ml in some cases (H8, L7). 

NS) (F) Hepatic Renal 1.04M 1.04 M (increased urinary protein, NaCN... 

Studies in experimental animals have also shown increased urinary protein accompanied or unaccompanied by histopathological changes of the kidneys following exposure to mirex (NTP 1990) or chlordecone (Larson et al. 1979b). Although these changes are not specific for mirex or chlordecone, measurement of these parameters may provide information about renal damage in exposed populations. 

Angiotensin-converting enzyme (ACE) inhibitors such as captopril exert a long-term reno-protective effect. Among other effects, they lower systemic blood pressure and renal plasma flow and effectively reduce urinary protein excretion. Renal delivery of ACE-inhibitors may increase this efficacy and reduce extra-renal side-effects. Renal targeting of an ACE-in-hibitor can also be useful in clarifying the contribution of local ACE inhibition to these reno-protective effects. 

Prednisolone can cause an abrupt rise in proteinuria in patients with nephrotic syndrome. A placebo-controlled study in 26 patients aged 18-68 years with nephrotic syndrome has clarified the mechanisms responsible for this (163). Systemic and renal hemodynamics and urinary protein excretion were measured after prednisolone (125 mg or 150 mg when body weight exceeded 75 kg) and after placebo. Prednisolone increased proteinuria by changing the size-selective barrier of the glomerular capillaries. Neither the renin-angiotensin axis nor prostaglandins were involved in these effects of prednisolone on proteinuria. 

This patient, who had autosomal dominant polycystic kidney disease (ADPKD), almost drowned and then developed ALPE. On July 20, 1990, he nearly drowned in the sea at 1500 hours, and was brought to our hospital by ambulance for dyspnea and severe loin pain at 1620 hours. On admission, metabolic acidosis was observed. His CRP, serum creatinine, CPK, amylase, and urinary protein levels were 1+, 1.5mg/dl, 116 U/l, 592IU/1 (derived from the salivary gland), and 2+, respectively. His body temperature was 37.7°C, and his blood pressure was 110/60 mmHg. His pulse and respiratory rate were 120/min and 22/min, respectively. Delayed CT 6h after the administration of contrast medium showed wedge-shaped contrast enhancement in the noncystic renal parenchyma (Fig. 34). On July 24, a bone scan with MDP revealed patchy lesions (Fig. 35). His serum creatinine level was 1.3 mg/dl, which had decreased to 1.0 mg/dl on July 27. The patient was then discharged. 

Murakami T, Itagaki A, Takahashi H (1988-1989) A change of urinary proteins from a glomerular pattern to a tubular pattern during a late diuretic phase of acute renal failure. Child Nephrol Urol 9 160-162... 

By age 11 years his renal function decreased, as measured by a creatinine clearance of 71 mL/min (normal is 105 mL/min). He also developed protein-losing nephropathy with a 24-hour urinary protein excretion of 600 mg that increased to 14 g after albumin infusions... 

Impaired renal function has rarely been caused by isotretinoin (82) and etretinate (83). Abnormalities in urinary proteins, inflammation of the urethral meatus, and nephrolithiasis have rarely occurred. Urethritis may occur more often than has been realized (SEDA-21,162) (84). 

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