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 kidneys are an important target for toxic effects of drug candidates. It is mandatory to select accurate, clinically relevant parameters in order to be in a position to detect putative nephrotoxic effects during the safety pharmacology programme. The glomerular filtration rate appears to be of major interest since it is associated with the definition of acute renal failure. Measurement of the renal blood flow, proteinuria, enzymuria, fractional excretion of sodium, etc. are also highly useful to detect any possible renal impact of a new compound. Although the rat is, by far, the most widely used animal species, there are no specific (clinically relevant) reasons to choose it. Various parameters may vary according to the species, sex, strain, age, etc. Since in most cases acute renal failure occurs following administration of drugs in patients with pre-existing risk factors, it is suggested that sensitized animal models be validated and used (salt depletion, dehydration, co-administration of pharmacologic agents, etc.).
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PMID:Renal safety pharmacology: value of sensitized experimental models. 1086 6

Renal involvement in 204 cases with multiple myeloma admitted over a 10-year period to this tertiary care center in north India was retrospectively examined. Renal involvement occurred in 55 cases (27%); the vast majority of whom (94.5%) had presented with renal failure and 7.3% had nephrotic syndrome. The diagnosis of multiple myeloma was made after admission in 51 of the 55 (92.7%) cases. Oliguria was seen in 23.6% and two-third patients required dialysis. Factors precipitating renal failure were identified in 53% and included dehydration (33%), hypercalcemia (24%), nephrotoxic drugs (16%), sepsis (9%), recent surgery (5%) and contrast media (2%), Severe anemia, hypercalcemia, Bence Jones proteinuria and skeletal abnormalities were more frequent in those with renal involvement. Patients with renal involvement were more likely to have a high tumor burden. The myeloma was of light chain type in 68% of those with renal involvement whereas IgG myeloma was commonest (57%) in those without evidence of renal disease. Renal histology was studied in 27 cases with myeloma cast nephropathy seen in over 60%. Tubulointerstitial nephritis was seen in 14% cases, 11% had amyloidosis, 7% had acute tubular necrosis and 3.6% each had nodular glomerulosclerosis and plasma cell infiltration. In 8 cases (14.6%), renal biopsy provided the first clue to the diagnosis of myeloma. Renal function improved in 33% cases. Only 22% of patients on dialysis survived over 6 months. Median survival in those with renal involvement was only 4 months. Development of unexplained renal failure in an elderly individual with normal sized kidneys, in association with disproportionate anemia even in the absence of skeletal lesions should alert the physician to the diagnosis of multiple myeloma.
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PMID:Renal involvement in multiple myeloma: a 10-year study. 1090 Nov 84

Proteinuria is a common finding in adults in primary care practice. An algorithmic approach can be used to differentiate benign causes of proteinuria from rarer, more serious disorders. Benign causes include fever, intense activity or exercise, dehydration, emotional stress and acute illness. More serious causes include glomerulonephritis and multiple myeloma. Alkaline, dilute or concentrated urine; gross hematuria; and the presence of mucus, semen or white blood cells can cause a dipstick urinalysis to be falsely positive for protein. Of the three pathophysiologic mechanisms (glomerular, tubular and overflow) that produce proteinuria, glomerular malfunction is the most common and usually corresponds to a urinary protein excretion of more than 2 g per 24 hours. When a quantitative measurement of urinary protein is needed, most physicians prefer a 24-hour urine specimen. However, the urine protein-to-creatinine ratio performed on a random specimen has many advantages over the 24-hour collection, primarily convenience and possibly accuracy. Most patients evaluated for proteinuria have a benign cause. Patients with proteinuria greater than 2 g per day or in whom the underlying etiology remains unclear after a thorough medical evaluation should be referred to a nephrologist.
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PMID:Proteinuria in adults: a diagnostic approach. 1101 62

We report on a 4-year-old girl with hyponatremic-hypertensive syndrome (HHS), a rare entity in childhood. The girl was referred to us from a local hospital with a history of recurrent fever, vomiting, and seizures. On admission she was markedly dehydrated. Initial investigations revealed severe hyponatremia (serum Na 120 mmol/l), hypochloremia (serum Cl 68 mmol/l), and mild hypokalemia (serum K 3.3 mmol/l), while serum calcium and magnesium were normal. Serum urea was 5 mmol/l and serum creatinine was 62 mumol/l. Despite hyponatremic dehydration, her urine output was high (2050 ml/24 h), as was her urinary sodium (168 mmol/24 h). She had massive transient proteinuria (maximal 1642 mg/24 h) while being severely hypertensive (blood pressure 210/160 mmHg). Further investigations revealed right kidney scarring, hyper-reflexive bladder dysfunction, massive brain infarcts, and myocardial left ventricular hypertrophy. Renal arteries were normal on arteriography. Blood pressure control resulted in normalization of serum and urinary electrolytes and decrease of proteinuria. Hyponatremia and transient massive proteinuria in this patient seem to be caused by high-pressure-forced diuresis due to malignant renoparenchymal hypertension.
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PMID:Hyponatremic hypertensive syndrome. 1114 28

A Multiple Myeloma (MM), IgG-lambda stage III-A was diagnosed in a 41-year-old-man. After VAD cycles IgG decreased from 7.5 to 2.4 g/dL. were mobilized with cyclophosphamide and 10 micrograms/Kg G-CSF. Three days after the collection of peripheral stem cell, the patient had fever, nausea, vomiting, liquid stools, shoulder and knee arthralgia and dehydration. Upper GI endoscopy showed esophageal candidiasis and ulcerative necrotic lesions both in stomach and duodenum; the biopsy confirmed necrosis. Simultaneously, the appearance of purpura with maculopapular lesions of diverse sizes appeared in the feet progressing to the limbs and trunk. Hematuria and proteinuria were also observed. Skin biopsy showed leukocytoclastic vasculitis. Renal biopsy showed focal and segmental glomerulonephritis. Serum ANCA, cryoglobulins, anti-HCV and RF were negative, and serum monoclonal IgG was 1290 mg/dL. Daily treatment with i.v. methylprednisolone pulses for 3 days improved skin lesions and digestive involvement. Macroscopic hematuria and proteinuria improved after two months of steroid treatment.
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PMID:[Severe Henoch-Schonlein purpura in a patient with multiple myeloma]. 1134 14

The unusual coincidence of Bartter syndrome and C1q nephropathy is described and the literature reviewed. An African-American girl presented at 4 years of age with acute hyponatremic dehydration and failure to thrive. Persistent hypokalemic alkalosis and secondary hyperaldosteronism were found. The case was atypical for Bartter syndrome in that proteinuria (0.19 g/day) was present. Renal biopsy showed juxtaglomerular hyperplasia and C1q nephropathy. Molecular analysis showed deletion of the renal chloride channel gene (CLCNKB) typical of autosomal recessive childhood Bartter syndrome. Chronic sodium and potassium chloride replacement therapy together with indomethacin normalized her metabolic status, and she experienced catch-up growth. Proteinuria persisted, however. This is the first documentation of C1q nephropathy, in mild form, complicating autosomal recessive Bartter syndrome. This case shows the importance of the renal biopsy and of molecular analysis in delineating the cause of atypical nephropathy associated with Bartter syndrome. These findings add to the evidence of a possible association between the congenital syndrome and acquired immune complex nephropathy.
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PMID:Bartter syndrome complicated by immune complex nephropathy. Case report and literature review. 1283 94

Early optimalization of the treatment of patients with chronic renal insufficiency can reduce morbidity and deaths. For each patient with a raised serum creatinine concentration, the creatinine clearance should be measured or calculated. When this is abnormal, the cause thereof should be investigated. Chronic renal insufficiency is often progressive, even when the initiating factors are no longer present. Progression can be delayed by treating the high blood pressure, proteinuria and hyperlipidemia by means of a restricted protein diet and advice not to smoke. Acute deterioration of an existing chronic renal dysfunction through dehydration and underfill or through the use of certain medications or toxic substances such as radio-opaque media should be avoided. In patients with chronic renal insufficiency specific attention should be paid not only to hypertension, lipid disturbances, smoking and weight, but also to the calcium-phosphate balance, anaemia and homocysteine levels. The blood pressure, oedema and weight of patients with a clearance between 30-59 ml/min should be checked 2-3 times a year, in addition to laboratory tests for Hb, Ht, creatinine, urea, potassium, calcium, phosphate, pH, bicarbonate and lipid spectrum. It is recommended that when creatinine clearance (< 50 ml/min) falls a nephrologist should be consulted at least once with respect to the strategy to be followed. Symptoms of chronic renal insufficiency can occur when the creatinine clearance is < 30 ml/min. This relates to: sodium retention, imbalances in the calcium and phosphate levels, anaemia, uraemia, water retention, potassium retention and metabolic acidosis. Referral should take place at a creatinine clearance of < or = 30 ml/min.
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PMID:[Treatment of patients with chronic renal insufficiency; a guideline for internists]. 1511 99

A 12-year-old girl, who had been diagnosed as having Cockayne syndrome (CS), was admitted for emaciation and dehydration. On admission the patient had mild chronic renal failure (glomerular filtration rate: GFR 50 mL/min) and hyperuricemia. After rehydration, allopurinol was commenced for her hyperuricemia. Then, her renal function rapidly deteriorated (GFR 20 mL/min) with enhancement of proximal tubular dysfunction and hypertension. A renal biopsy showed that the patient had acute tubulointerstitial nephritis (ATIN). Based on this diagnosis, allopurinol was stopped and prednisolone was started (2 mg/kg per day), following which the renal tubular function improved. However, the proteinuria intensified to become nephrotic syndrome. After 1 month the patient developed a gastric ulcer. Famotidine was commenced but GFR deteriorated and renal proximal tubular dysfunction re-occurred. The renal pathology was evaluated by referring to the previous reports of renal pathology in CS. It is suggested that rapid deterioration of the renal function in CS patients might be the result of ATIN. In addition, the present nephrotic syndrome seemed to be accompanied by ATIN, as in other reports.
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PMID:Cockayne syndrome with recurrent acute tubulointerstitial nephritis. 1704 Feb 91

Mesalazine is a first-line drug in pediatric inflammatory bowel disease, and is effective as primary treatment and maintenance therapy. It's usually well tolerated, but various side effects have been described. A 15-year-old female with ulcerative colitis developed polyuria, polydipsia, vomiting, and fatigue. She was receiving mesalazine (500 mg, thrice daily, p.o.) and prednisolone for 4 months. She was detected as acute tubular injury as she had dehydration, acidosis, hypostenuria, hematuria, proteinuria, low levels of potassium, uric acid and bicarbonate. These findings were attributed to interstitial nephritis as a side effect of mesalazine, however as renal biopsy was disapproved by the parents, it was not confirmed. After discontinuation of mesalazine her renal tubular functions improved. Potassium and phosphorus supplements were stopped after 7 months, although she had to continue bicarbonate supplementation. We conclude that regular renal screening is important in patients receiving 5-ASA therapy to prevent rare but serious complications, such as interstitial nephritis sometimes leading to chronic renal failure.
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PMID:Acute tubular injury associated with mesalazine therapy in an adolescent girl with inflammatory bowel disease. 1740 67

This study was designed to test the hypothesis that blockade of angiotensin II effects during renal development accelerates the aging-related changes in renal hemodynamics and proteinuria, and that these changes are sex dependent. It has also been examined whether the deterioration of urinary concentrating ability elicited by angiotensin II blockade is sex and/or aging dependent. Newborn Sprague-Dawley rats were treated with vehicle or an AT(1) angiotensin II receptor antagonist (ARA) during the first 14 postnatal days. Blood pressure, glomerular filtration rate, proteinuria, and urinary concentrating ability in response to dehydration were examined in conscious rats at 3 and 11 mo of age. ARA treatment elicited a similar increment in blood pressure in males and females that was greater (P < 0.05) at 11 than at 3 mo of age. Glomerular filtration rate only decreased (P < 0.05) in 11-mo-old male ARA-treated rats (0.59 +/- 0.07 vs. 0.80 +/- 0.07 ml.min(-1).g(-1) in control group). At 3 mo of age, proteinuria increased in male (107%) but not in female ARA-treated rats. However, at 11 mo of age, proteinuria increased in both sexes, but the increment was greater (P < 0.05) in male (244%) than in female (138%) ARA-treated rats. Renal ability to concentrate urine in response to prolonged water dehydration was only reduced in ARA-treated males. The reduction of urinary concentrating ability was accentuated by aging. Therefore, we conclude that blockade of angiotensin II effects during renal development elicits an important deterioration of cortical and medullary function that is sex and aging dependent.
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PMID:Sex and age differences of renal function in rats with reduced ANG II activity during the nephrogenic period. 1744 28


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