Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The interaction of the endogenous vasoconstrictors endothelin (ET), angiotensin II (Ang II) and catecholamines with the kallikrein-kinin-, prostaglandin and renin-aldosterone systems in the pathogenesis of acute renal failure (ARF) is still to be defined. In 18 anesthesized pigs the influence of i.v. bolus applications of ET (2 micrograms/kg), Ang II (10 micrograms/kg) and norepinephrine (NE; 20 micrograms/kg) on hemodynamics, plasmatic coagulation and fibrinolysis system, prostaglandins and renal function was studied. ET induced a biphasic change in blood pressure, starting with an initial short-lasting reduction followed by a long-lasting elevation of systolic and diastolic blood pressure. Endothelin bolus resulted in a significant increase of 6-keto-PGF1 alpha, PGE2 and TXB2 plasma levels (P < 0.05 against preinjection values), whereas prostaglandins remained unchanged in the Ang II and NE groups. There was a distinct correlation between the plasma ET and 6-keto-PGF1 alpha levels (r = 0.82). In contrast to Ang II or NE, ET induced a shortening of the activated partial thromboplastin time (aPTT) and increase of antithrombin III levels (ATIII), fibrin monomers (FM), prekallikrein (PKK) and factor VIII activity at the beginning. Finally a pronounced decrease of ATIII, FM and PKK occurred, indicating a consumptive coagulopathy. At the end of the experiment, elevated plasma renin activity and pCO2, significantly decreased creatinine clearance, blood pH, pO2, base excess, HCO3-, oxygen saturation (P < 0.01), a distinct glomerular proteinuria, and a final anuria were observated. These results reveal that ET activates the plasmatic coagulation system and induces an ARF accompanied by impairment of pulmonary function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of endothelin on hemodynamics, prostaglandins, blood coagulation and renal function. 775 79

Oral calcium supplementation is reported to have phosphate-binding and antihypertensive effects. Since both phosphate binders and antihypertensive agents are reported to attenuate renal injury, we studied the effect of oral calcium carbonate (CaCO3) administration on the course of renal deterioration using doxorubicin-induced renal failure in rats treated with deoxycorticosterone acetate and salt for 10 weeks. Rats were divided into four groups: the CaCO3 (6.0 g/kg/d) group (n = 12), the aluminum hydroxide (Al(OH)3; 6.0 g/kg/d) group (n = 11, as a phosphate-binder control), the hydralazine (10 mg/kg/d) group (n = 11, as an antihypertensive control), and the control group (n = 12). All agents were given as a mixed chow diet. Blood pressure and urinary protein excretion progressively increased in the control rats. CaCO3 and hydralazine lowered blood pressure, but Al(OH)3 did not (185 +/- 4 mm Hg, control; 160 +/- 5 mm Hg, CaCO3; 171 +/- 8 mm Hg, Al(OH)3; 156 +/- 5 mm Hg, hydralazine at week 10). Proteinuria was reduced in the rats treated with CaCO3 and Al(OH)3 compared with those without the treatment (986 +/- 86 mg/d, control; 551 +/- 54 mg/d, CaCO3; 527 +/- 31 mg/d, Al(OH)3; and 955 +/- 68 mg/d, hydralazine at week 10). Serum phosphate concentration and calcium phosphate products also were significantly lower in both the CaCO3 and Al(OH)3 groups than in the control group. At week 10, increased serum urea nitrogen, impaired renal function, and glomerular sclerosis present in the control group were significantly attenuated in both in the CaCO3 and Al(OH)3 groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oral calcium carbonate administration ameliorates the progression of renal failure in rats with hypertension. 777 88

To assess renal function changes in acute nephrotoxicosis in dogs, the development and evolution of renal damage during induced citrinin intoxication were studied. Six dogs (experimental group) were given 10 mg citrinin/kg/BW every 24 h during 2 d, and 5 dogs (control group) received exclusively the diluent (1 ml 1% sodium carbonate/kg/BW/d for 2 d). The dogs were daily submitted to physical examination, urinalysis and blood biochemistry analyses (blood urea, serum creatinine, potassium, sodium and glucose) during 2 w. The citrinin-induced renal lesions were mainly in the proximal convoluted tubule and characterized by proteinuria, glucosuria and the presence of numerous granular casts in the urine sediment; these could be detected before elevations in blood urea and creatinine. Glucosuria was the earliest abnormality found and lasted 5 d, while proteinuria and cylindruria were observed from days 1 to 5 and from days 1 to 15, respectively. The glomerular filtration rate was slightly affected as observed by blood urea and creatinine elevations from days 2 to 5. Urine analysis is a useful tool for the evaluation of nephrotoxicity since most nephrotoxins act primarily on the proximal convoluted tubule.
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PMID:Experimental citrinin nephrotoxicosis in dogs: renal function evaluation. 847 Mar 56

Chronic vascular rejection (CR) is the commonest cause of renal transplant loss, with few clues to etiology, but proteinuria is a common feature. In diseased native kidneys, proteinuria and progression to failure are linked. We proposed a pathogenic role for this excess protein at a tubular level in kidney diseases of dissimilar origin. We demonstrated in both nephrotic patients with normal function and in those with failing kidneys increased renal tubular catabolism and turnover rates of a peptide marker, Aprotinin (Apr), linked to increased ammonia excretion and tubular injury. These potentially injurious processes were suppressed by reducing proteinuria with Lisinopril. Do similar mechanisms of renal injury and such a linkage also occur in proteinuric transplanted patients with CR, and if so, is Lisinopril then of beneficial value? We now examine these aspects in 11 patients with moderate/severe renal impairment (51CrEDTA clearance 26.2+/-3.3 mL/min/1.73 m2), proteinuria (6.1+/-1.5 g/24 h) and biopsy proven CR. Lisinopril (10-40 mg) was given daily for 2 months in 7 patients. Four others were given oral sodium bicarbonate (Na HCO3) for 2 months before adding Lisinopril. Renal tubular catabolism of intravenous 99mTc-Apr (Apr* 0.5 mg, 80MBq), was measured before and after Lisinopril by gamma-ray renal imaging and urinary radioactivity of the free radiolabel over 26 h. Fractional degradation was calculated from these data. Total 24 h urinary N-acetyl-beta-glucoaminidase (NAG) and ammonia excretion in fresh timed urine collections were also measured every two weeks from two months before treatment. After Lisinopril proteinuria fell significantly (from 7.8+/-2.2 to 3.4+/-1.9 g/24 h, p<0.05). This was associated with a reduction in metabolism of Apr* over 26 h (from 0.5+/-0.05 to 0.3+/-0.005% dose/h, p < 0.02), and in fractional degradation (from 0.04+/-0.009 to 0.02+/-0.005/h, p<0.01). Urinary ammonia fell, but surprisingly not significantly and this was explained by the increased clinical acidosis after Lisinopril, (plasma bicarbonate fell from 19.1+/-0.7 to 17.4+/-0.8 mmol/L, p < 0.01), an original observation. Total urinary NAG did fall significantly from a median of 2108 (range 1044-3816) to 1008 (76-2147) micromol/L, p < 0.05. There was no significant change in blood pressure or in measurements of glomerular hemodynamics. In the 4 patients who were given Na HCO3 before adding Lisinopril, both acidosis (and hyperkalemia) were reversed and neither recurred after adding Lisinopril. These observations in proteinuric transplanted patients after Lisinopril treatment have not been previously described.
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PMID:Renal tubular peptide catabolism in chronic vascular rejection. 1149 66

Lithium carbonate has been recognized to induce several renal side effects, including the nephrotic syndrome. This is a report of an 11-year-old, prepubertal boy with a mood disorder treated with lithium who presented with edema, bilateral pulmonary effusions, proteinuria, and hypoalbuminemia. Renal biopsy revealed pathologic changes consistent with minimal change disease. These symptoms normalized after lithium discontinuation.
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PMID:Lithium-induced nephrotic syndrome in a prepubertal boy. 1843 18

Here we describe a 65-year-old Japanese man with chronic renal failure (CRF) and a large, dense, calcified abdominal mass. The patient had a history of proteinuria, which was diagnosed as focal glomerulosclerosis. This diagnosis was confirmed by renal biopsy in 2002, with worsening renal function by July 2005 when a large area of calcification was detected on abdominal radiography, which further increased in size on follow-up radiography in December 2006. The calcified mass was surgically resected and histopathologically diagnosed as myxoid-type liposarcoma composed of dedifferentiated, myxoid, and well-differentiated components with areas of osseous metaplasia. Soft tissue calcifications and ossifications are often benign, but malignant tumors should be considered when the calcified mass is retroperitoneal, occurs in a patient with no history of chronic infection, and is not located near a large joint or associated with administration of calcium carbonate or a vitamin D derivative.
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PMID:A large calcified retroperitoneal mass in a patient with chronic renal failure: liposarcoma with ossification. 1988 3

Nephrotic syndrome increases L-thyroxine requirements because of urinary loss of free and protein-bound thyroid hormones. We report 2 hypothyroid patients referred to us because of high serum TSH, even though the L-thyroxine daily dose was maintained at appropriate levels or was increased. The cause of nephrotic syndrome was multiple myeloma in one patient and diabetic glomerulosclerosis in the other patient. As part of the periodic controls for diabetes, urinalysis was requested only in the second patient so that proteinuria could be detected. However, as in the first patient, facial puffiness and body weight increase were initially attributed to hypothyroidism, which was poorly compensated by L-thyroxine therapy. In the first patient, the pitting nature of the pedal edema was missed at the initial examination. An endocrinologist consulted over the phone by the practitioner hypothesized some causes of intestinal malabsorption of L-thyroxine. This diagnosis would have been accepted had the patient continued taking a known sequestrant of L-thyroxine, i.e. calcium carbonate. The diagnostic workup of patients with increasing requirements of L-thyroxine replacement therapy should not be concentrated on the digestive system alone. Careful history taking and physical examination need to be thorough. Endocrinologists should not forget nephrotic syndrome that, in turn, can be secondary to serious diseases.
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PMID:Do Not Forget Nephrotic Syndrome as a Cause of Increased Requirement of Levothyroxine Replacement Therapy. 2628

Particularly because the risk of harm cannot be safely excluded, the use of phosphate binders in chronic kidney disease (CKD) patients demands caution. Yet, the clinical inertia concerning phosphate burden is unjustified. Inorganic, phosphate esters added to preserve food represent an important component of dietary phosphate load. These compounds are easily absorbable and have a measurable effect on serum phosphate, and therefore their use should be avoided in CKD patients. The ongoing CKD Optimal management with Binders and NicotinamidE (COMBINE) study, applying chelation by phosphate binders and intestinal Na-P channel blockade by nicotinamide, will establish whether this combination may effectively reduce serum phosphate and fibroblast growth factor 23 in pre-dialysis CKD patients and produce improvements in surrogate measures of cardiovascular and renal damages. On the other hand, the ANSWER study will ascertain whether phosphate reduction by sevelamer carbonate may have an antiproteinuric effect in CKD patients with residual proteinuria despite effective blockade of the renin-angiotensin system. At this stage of knowledge, the use of phosphate binders in pre-dialysis CKD patients cannot be recommended. Ongoing studies will tell us whether the application of these drugs may have beneficial health effects in CKD patients at the pre-dialysis stage.
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PMID:Moderator's view: Phosphate binders in chronic kidney disease patients: a clear 'No' at the moment, but stay tuned. 2668 48


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