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)

THREE GROUPS OF PATIENTS: A with normal glomerular filtration rate, B with moderate and C with advanced renal damage, were dehydrated and fasted for 30 hours. At regular intervals measurements were taken of urine osmolality, urine specific gravity and serum osmolality. The time required to reach maximum urine osmolality varies with the degree of dehydration and inversely with the severity of kidney damage. In patients with normal glomerular filtration rate, maximum urine osmolality is not attained by 30 hours of dehydration. Thus, for shorter periods, all "normal ranges" of concentrating capacity must be related to specific durations of dehydration. Carefully measured urine specific gravities parallel urine osmolalities closely, especially when proteinuria and glucosuria are absent. The measurement of U/P osmolality ratio offers no clinical advantage in the assessment of renal concentration capacity over the measurement of urine osmolality alone. In Group A, hypertensives achieved higher urine concentrations than did the nonhypertensives under identical test conditions. A normal range for renal concentrating capacity has been presented.
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PMID:A standardized test of renal concentrating capacity in adults with some results in essential hypertension. 536 6

The process of intraerythrocytic gelling of haemoglobin S is exacerbated by physiochemical and circulatory conditions which dominate in the renal medulla. In the first few years of life, the sickle cell disturbance is reversible by exchange transfusions. At about the age of 15, this is no longer reversible in homozygotes and is replaced by anatomical lesions which gradually destroy the renal functional capacity for concentrating urine, for excreting H+ and K+ ions and for secreting uric acid. The crises are acute rheological events which temporarily accentuate these disorders which appear to be the combined result of hyperviscosity and vascular occlusions. As the occurrence of hematuria and urinary infections is necessarily organically linked to the parenchymatous lesions, their frequency and severity pose great problems concerning treatment. Recent works emphasize the frequency and severity of renal disorders in sickle cell patients during the period of life which is over 30 years. A preventive disposition must be maintained from childhood: restriction of the use of nephrotoxic drugs, reduction of the frequency of crises, dehydration and urinary infections, and subsequently regular observation of kalemia, uricemia and proteinuria.
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PMID:[Anatomical and pathophysiological bases of renal disorders in sickle cell syndrome patients and carriers of the trait]. 635 9

Renal failure was diagnosed in 22 young Doberman Pinscher dogs. The clinical findings were anorexia, weight loss, vomiting, lethargy, polydipsia, polyuria, and dehydration. Laboratory findings were azotemia, hyperphosphatemia, lymphopenia, nonregenerative anemia, hypercholesterolemia, and proteinuria. The kidneys were characterized pathologically by glomerular sclerosis, cystic glomerular atrophy, tubular dilatation, tubular atrophy, mononuclear interstitial inflammation, interstitial fibrosis, interstitial mineralization, and hyperplasia of the collecting duct epithelium.
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PMID:Juvenile renal disease in Doberman Pinscher dogs. 683 84

The renal involvement in a multiple myeloma case (MM) has a frequency of 50% and causes a worsening of the disease with a survival average of about 12 months. Myeloma cast nephropathy (MCN) represents the more frequent clinic, histological form of nephropathy in course of MM and it evolves when monoclonal light free chain deposit in the renal tubules together with some other worse cases like dehydration and/or hypercalcaemia. We analyze here the clinical and renal histological features of eight patients treated for acute renal failure found in MCN in course of MM grade B. This was discovered through renal bioptic check-up. We have evaluated the Bence-Jones proteinuria, the recurrence of the condition of risk and the course of the renal failure of these patients also in order to treat the hematological illness.
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PMID:[Acute kidney failure in the patient with multiple myeloma. An analysis of the authors' personal cases]. 775 76

Exercise induces profound changes in renal haemodynamics and protein excretion. The rate of ultrafiltration across the glomerular capillary is determined by the imbalance between the transcapillary hydraulic and colloid osmotic pressure gradients. Despite a major reduction in the renal plasma flow, the filtration fraction can double with maximal exercise, preserving the transfer of metabolites or substances through the glomerulus. Tubular processes and excretion rates are modified by exercise. Despite large increases in plasma lactate during strenuous exercise, renal excretion plays a limited role in lactate metabolism. Apparently, the mechanism of transcellular transport of lactate is saturated during severe exercise. Urea reabsorption is enhanced during prolonged exercise, and this process may act to limit the dehydration of an individual. As uric acid transport is also carrier-mediated, it appears that there is no saturation of the carrier system during prolonged exercise. Postexercise proteinuria is directly related to the intensity of exercise rather than to its duration. This excretion of excess proteins is a transient state with a half-time decay of about 1 hour. The increased clearance of plasma proteins suggests an increased glomerular permeability and a partial inhibition of tubular reabsorption. Studies suggest that exercise decreases the glomerular electrostatic barrier and facilitates transfer of macromolecules. Postexercise proteinuria appears to be age-dependent. Nephropathy is a common observation in the diabetic patient. In young and adult diabetic patients, exhaustive physical exercise does not provoke an enhanced dysfunction of the kidney to what is already found in healthy individuals. Heart and kidney transplant patients have a lesser postexercise proteinuria as compared with healthy individuals.
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PMID:Kidney function during exercise in healthy and diseased humans. An update. 788 56

The retrospective analysis had been performed on 3480 newborns weighted more than 1001 g, over the period of thirty one months. There was evaluated the frequency (1.25%), and clinical manifestation of the disease in newborns. Male and full term infants suffered from the disease more frequently then other evaluated infants. About half of cases were asymptomatic in the beginning of disease, and in the majority part of them, course of illness were non-characteristic. There was observed generalised oedema and swellings, irritability, intensive jaundice, dehydration, fever and poor peripheral perfusion. Laboratory findings manifested: anemia, hypoglycemia, higher WBC, metabolic acidosis, and especially hyperbilirubinemia, and in urine: pyuria and proteinuria mainly. In most cases of the disease urea and creatinine level in the serum were normal. The most dominant pathogenic agent was E. coli (above 72%).
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PMID:[Urinary tract infections in newborns]. 814 52

The renal concern in a multiple myeloma (MM) case has a frequency of 50% and causes a worsening of the disease with a survival average of about 12 months. The monoclonal light free chains (CLL) produced in excess by the plasmacytes are present in the urine as proteinuria of Bence Jones (PBJ) in 60-70% of patients affected by MM. They represent the major pathogenetic factor of the nephropathy in course of MM as they can deposit in shape of intratubular "casts" in the myeloma casts nephropathy (MCN). In some worse cases, dehydration or hypercalcaemia can cause an irreversible acute renal insufficiency (RI). It is therefore important in a patient affected with MM with PBJ to prevent, locate and opportunely treat these situations which worsen the nephropathy. Beside the tubular cast nephropathy, the CLL "accumulate" in the kidney even though with a lower frequency compared to MCN, in the light chains deposition disease (LCDD) and in the amyloidosis AL (AL). LCDD is characterized by a deposit of nodular amorphous materials PAS positive in the glomerulus and sometimes even in the tubulus. It usually presents itself as a chronic RI and a proteinuria causing nephrotic syndrome (NS). This quickly evolves into uraemia and its evolution can be lessened by the MM treatment. AL in course of MM also reveals with a chronic RI and NS. CLLs deposit in the typical fibrillar structure, on the vessel walls, in the glomerulus, in the mesangium and can be marked out with the Congo red colouring and the subsequent green birefringence through microscope with polarized light. Prognosis of AL is extremely severe and no benefit is given by the treatment of the hematological illness. It is therefore absolutely necessary to study the renal histology through biopsy when MM is grade B, that is, with serumal creatinine above 2 mg/dl as: MCN imposes the MM treatment programme in order to reduce the tubular excess of PBJ and to attempt to make RI reversible; MCN with tubular atrophy and interstitial fibrosis results in an unfavourable prognosis as it expresses a nephropathic irreversibility due to the loss nephrons. It will therefore necessary to start on a renal substitutional treatment programme. Renal damage in course of MM is not always tubular, rather an unexpected glomerular damage of LCDD or amyloidosis AL type can be found.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The kidney in multiple myeloma. The physiopathological and clinical aspects]. 818 90

Nitrogen retention of various intensity was found in 61 patients with multiple myeloma. In seven (11%) of them the disturbances of the depurative renal function manifested as acute renal failure (ARF). The syndrome was characterised in etiologic, pathogenetic, clinical, therapeutic and prognostic aspects. ARF in the study developed on the background of a light chain proteinuria in patients with hypercalcemia, dehydration, radiocontrast studies, blood loss, surgical interventions, and severe infections. Following conservative treatment, the renal function normalized in one patient, a gradual transition to chronic renal failure was observed in five patients, and lethal outcome in one patient. The average survival rate after ARF was 8 months (1-13 months).
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PMID:Acute renal failure in patients with multiple myeloma. 900 62

A case of significant proteinuria occurred as a result of bilateral renal vein thrombosis secondary to dehydration, which resolved after treatment with urokinase. The patient developed nausea and vomiting from viral gastroenteritis with subsequent volume contraction. He later noted the onset of aching lower abdominal and flank pain. On admission, he was noted to have a serum creatinine of 1.7 mg/dL, and 4+ proteinuria on urinalysis. A 24-hour urine collection showed 2.34 g protein. A renal venogram showed bilateral renal vein thrombosis (RVT) without involvement of the inferior vena cava. Therapy was initiated with heparin at 1,000 U/hr, followed by intravenous (IV) urokinase, 4,400 U/kg bolus, followed by 4,400 U/kg/hr with continuous infusion for 12 hours. A repeat renal venogram done at this time showed partial resolution of thrombosis bilaterally. A second 12-hour infusion of urokinase at 5,000 U/kg/hr was performed; at this time, the patient reported resolution of his flank and abdominal pain. A repeat 24-hour urine collection showed 60 mg protein with a normal creatinine clearance. Levels of antithrombin III, protein C, and protein S were all normal. A renal biopsy was performed and showed normal histology on light, immunofluorescent, and electron microscopic evaluation. The patient has done well on no therapy and has had no recurrence of thrombosis or proteinuria after 2.5 years. This is a US government work. There are no restrictions on its use.
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PMID:Resolution of proteinuria secondary to bilateral renal vein thrombosis after treatment with systemic thrombolytic therapy. 910 53

Protein alteration resulting from a nonenzymatic reaction between ambient glucose and primary amino groups on proteins to form glycated residues called Amadori products is termed the Maillard reaction. By dehydration and fragmentation reactions, Amadori products are transformed to stable covalent adducts called advanced glycosylation end products (AGEs). In diabetes, accelerated synthesis and tissue deposition of AGEs is proposed as a contributing mechanism in the pathogenesis of clinical complications. Uremia in diabetes is associated with both a high serum level of AGEs and accelerated macro- and microvasculopathy. Diabetic uremic patients accumulate advanced glycosylated end products in "toxic" amounts that are not decreased to normal by hemodialysis or peritoneal dialysis but fall sharply to within the normal range within 8 h of restoration of half-normal glomerular filtration by renal transplantation. It follows that the higher mortality of hemodialysis-treated diabetic patients compared with those given a renal transplant may relate, in part, to persistent AGE toxicity. Pharmacologic prevention of AGE formation is an attractive means of preempting diabetic microvascular complications because it bypasses the necessity of having to attain euglycemia, an often unattainable goal. Pimagidine (aminoguanidine) interferes with nonenzymatic glycosylation and reduces measured AGE levels leading to its investigation as a potential treatment. The mechanism by which pimagidine prevents renal, eye, nerve, and other microvascular complications in animal models of diabetes is under investigation. Separate multicenter clinical trials of pimagidine in type 1 and type 2 diabetes, where proteinuria is attributable to diabetic nephropathy, are in progress. The effect of treatment on the amount of proteinuria, progression of renal insufficiency, and the course of retinopathy will be monitored.
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PMID:Advanced glycosylated end products and hyperglycemia in the pathogenesis of diabetic complications. 1009 2


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