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 first two cases outlined above with intractable massive proteinuria and uremia, were followed and treated with standard medical therapy and dialysis. After a period of study and demonstration of clinical deterioration both patients were given solutions containing sodium mercaptomerin. Within days there was a decline in urine protein excretion and a variable increase in serum protein concentration. The patients demonstrated an increase in blood pressure, which made hemodialysis treatment possible. No deleterious effects from the mercury salts were noted. These observations suggest that in selected cases nephrotoxic agents may be of value in decreasing massive proteinuria, and improving protein homeostasis in uremic patients. The ideal agent should be non-toxic to other organs and produce selective renal ablation (15). Although mercury is not the ideal agent, in these cases it did not produce observable side effects. This new method, applicable to dialysis patients with massive proteinuria, and of help in the control of uncontrollable hypertension in uremia, is an interesting new approach for our therapeutic armamentarium.
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PMID:Medical nephrectomy: the use of metallic salts for treatment of end stage massive proteinuria and renal hypertension. 633 53

Diabetic nephropathy has evolved into the single most prevalent cause of uremia among patients sustained by the United States End Stage Renal Disease program. Clarification of the natural history of kidney involvement and insufficiency in Type I and II diabetes has improved substantially over the past 5 years. However, it remains a poorly understood and relatively underreported morbid entity. This report reviews the problem, then reconstructs the natural history of diabetic nephropathy by studying the course of 50 Type I and Type II uremic diabetics treated with hemodialysis at The Long Island College Hospital. It traces the various stages from hyperglycemia to proteinuria to renal failure, and then reports morbidity, including cardiac, eye, stroke, and amputation complications. A new paradox is herein reported--the unpredictable insulin requirement, including new insulin need for the first time once hemodialysis was begun, in 8 of 50 patients studied.
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PMID:The natural history of diabetic nephropathy: unpredictable insulin requirements--a further clue. 636 68

Ten patients with clinical and laboratory features of acquired immune deficiency syndrome (AIDS) underwent renal ultrasonography prior to biopsy because of proteinuria, azotemia, or uremia. Four patients had a history of intravenous heroin abuse and were considered separately so as to exclude it as a cause of nephropathy. Histological examination revealed focal segmental glomerulosclerosis (FSGS), which in patients with AIDS is characterized by rapid progression to severe uremia (though FSGS can also occur in several other forms of renal disease). The authors recommend that AIDS-associated FSGS be considered as a cause of type I parenchymal disease and suggest that serial sonograms may be useful in monitoring progressive renal involvement.
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PMID:Renal ultrasound in acquired immune deficiency syndrome. 638 12

We report five cases of crescentic IgA nephropathy. All are males, 16-60 years of age. One case each came to medical attention with uremia, nephrotic syndrome, and gross hematuria; two cases presented with microhematuria and proteinuria on routine urinalysis. All had hypertension, azotemia (serum creatinine 1.6-9.4 mg/dl), proteinuria (greater than 6 g/24 hr in four cases), hypoalbuminemia (less than 3 g/dl), and hematuria (gross in two cases). All progressed to end-stage renal failure renal failure ending in dialysis (three cases) or death from unrelated causes (two cases). Prednisone, 60 mg/day for 1 month in two patients (with two 1-g doses of iv methylprednisolone in 1 case) did not improve the serum creatinine level, but one patient subsequently experienced a less rapid fall in renal function. A crescentic glomerulonephritis was present in all biopsies (crescents in 31-80% of glomeruli; mean, 50%). The size and stage of the crescents were variable. Numerous glomeruli had focal or diffuse sclerosis. In all cases, there was a 3 or 4+ deposition of IgA. Low-intensity staining for IgG and IgM was noted in four and three patients, respectively. On electron microscopy, dense granular mesangial deposits were noted in all cases and in four patients capillary subepithelial deposits were also observed. This form of IgA nephropathy is not common, but some studies indicate that it may occur in about 5% of patients with IgA nephropathy.
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PMID:Crescentic IgA nephropathy. 639 83

Alterations in renal function and structure are found even at the onset of diabetes mellitus. Studies performed over the last decade now allow definition of a series of stages in the development of renal changes in diabetes. Such a classification may be useful both in clinical work and in research activities. Stage 1 is characterized by early hyperfunction and hypertrophy. These changes are found at diagnosis, before insulin treatment. Increased urinary albumin excretion, aggravated during physical exercise, is also a characteristic finding. Changes are at least partly reversible by insulin treatment. Stage 2 develops silently over many years and is characterized by morphologic lesions without signs of clinical disease. However, kidney function tests and morphometry on biopsy specimens reveal changes. The function is characterized by increased GFR. During good diabetes control, albumin excretion is normal; however, physical exercise unmasks changes in albuminuria not demonstrable in the resting situation. During poor diabetes control albumin excretion goes up both at rest and during exercise. A number of patients continue in stage 2 throughout their lives. Stage 3, incipient diabetic nephropathy, is the forerunner of overt diabetic nephropathy. Its main manifestation is abnormally elevated urinary albumin excretion, as measured by radioimmunoassay. A level higher than the values found in normal subjects but lower than in clinical disease is the main characteristic of this stage, which appeared to be between 15 and 300 micrograms/min in the baseline situation. A slow, gradual increase over the years is a prominent feature in this very decisive phase of renal disease in diabetes when blood pressure is rising. The increased rate in albumin excretion is higher in patients with increased blood pressure. GFR is still supranormal and antihypertensive treatment in this phase is under investigation, using the physical exercise test. Stage 4 is overt diabetic nephropathy, the classic entity characterized by persistent proteinuria (greater than 0.5 g/24 h). When the associated high blood pressure is left untreated, renal function (GFR) declines, the mean fall rate being around 1 ml/min/mo. Long-term antihypertensive treatment reduces the fall rate by about 60% and thus postpones uremia considerably. Stage 5 is end-stage renal failure with uremia due to diabetic nephropathy. As many as 25% of the population presently entering the end-stage renal failure programs in the United States are diabetic. Diabetic nephropathy and diabetic vasculopathy constitute a major medical problem in society today.
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PMID:The stages in diabetic renal disease. With emphasis on the stage of incipient diabetic nephropathy. 640 Jun 70

In 1968 there was an epidemic outbreak of acute poststreptococcal glomerulonephritis in Maracaibo during which 384 cases were hospitalized. Of these cases, 120 were recalled in 1974 and the results of their investigations were reported. The present work concerns 71 patients from this group followed for 11-12 years and studied with measurement of creatinine clearance (CCr), protein excretion and urine sediment analyses. Measurements of serum immunoglobulins, cryoglobulins, C3 levels and rheumatoid factor titers were also made. One patient developed uremia and is in chronic dialysis. Persistent abnormalities were detected in 21.1% of the patients. Depressed creatinine clearance was found in 12.6% of the patients and proteinuria (0.5-2.0 g/day) in 11.2%. Microscopic hematuria occurred in 4.1%. Only 2 patients wer hypertensive. Transient serological abnormalities were seen in 36 patients: elevated IgG levels in 27, serum cryoglobulins in 17 and a low C3 level in 1 patient. Cryoglobulins were found in 50% of the patients with abnormal renal findings and in 22.9% of the patients with normal renal function and urine sediment. Children (at the time of the epidemic) had urinary abnormalities less frequently (16.1%) than did adults (55.5%). Of 9 patients who had been found abnormal five years before, 3 were improved or normal, 3 were stable and 3 showed progressive disease. our studies indicate that uremia is rare in the first decade after epidemic poststeptococcal glomerulonephritis. Nevertheless, the increasing incidence of depressed renal function dictates the need for continued follow-up of this group of patients.
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PMID:Long-term prognosis of epidemic poststreptococcal glomerulonephritis in Maracaibo: follow-up studies 11-12 years after the acute episode. 724 27

Dietary phosphorus restriction (PR) prevents uremia in rats with nephrotoxic serum nephritis (NSN). One possible mechanism by which PR could be protective would be through the suppression of parathyroid hormone. To evaluate this possibility two separate protocols were designed. In the first rats were thyroparathyroidectomized (TPTX) before (n = 11) or 5 wk after (n = 7) NSN induction and compared to sham-operated parathyroid intact rats with NSN (n = 12). At the end of the 23-wk study, intact rats were azotemic, plasma creatinine 3.80+/-0.81 mg/100 ml vs. 0.65+/-0.07 for TPTX rats (P < 0.001). During the study 75% of intact rats died of uremia in contrast to none of the TPTX rats (P < 0.001). Renal histological damage was greatly diminished and calcification prevented in TPTX rats. The proteinuria of the heterologous phase was unaffected, but the protein excretion and hypertriglyceridemia (HTG) of the autologous phase were markedly decreased in the TPTX rats. The degree of HTG and proteinuria had a high positive correlation (P < 0.001). Late TPTX also produced significant decreases in proteinuria and HTG regardless of the degree of azotemia, and prevented azotemia if the plasma creatinine at the time of TPTX was </=0.85 mg/100 ml. In additional studies selective parathyroidectomy (PTX) was performed. The adequacy of this procedure was documented by showing a similar fall in plasma Ca and urinary cyclic AMP in PTX animals as found in TPTX animals. However, selective PTX had no effect on proteinuria, histologic damage, or functional deterioration. These studies further showed that early, histologic damage and functional deterioration preceeded renal parenchymal calcification. Because animals were pair fed and both groups were given 1,25-dihydroxycholecalciferol to normalize serum Ca and P levels these studies exclude alterations in plasma Ca and P levels, dietary intake, urinary P excretion, and vitamin D administration in promoting the protective effect of TPTX on renal function. We conclude that TPTX is equally effective in preventing functional deterioration and more effective in reducing proteinuria in NSN than PR. The mechanism of this protective effect remains to be elucidated, since it does not primarily involve either the elimination of parathyroid hormone or the prevention of renal parenchymal calcification.
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PMID:Effect of thyroparathyroidectomy and parathyroidectomy on renal function and the nephrotic syndrome in rat nephrotoxic serum nephritis. 727 65

Microangiopathic hemolytic anemia and thrombocytopenia secondary to disseminated intravascular coagulation is a well-described complication of widely metastatic carcinoma. The authors report four cases of gastric carcinoma, one case of colon cancer, and one case of adenocarcinoma of unknown primary in which the patient developed a syndrome analogous to thrombotic thrombocytopenic purpura, consisting of microangiopathic hemolytic anemia, thrombocytopenia, and renal failure without definite evidence of disseminated intravascular coagulation. In contrast to previous reports, postmortem examination in three of the cases revealed no recurrence or only microscopic foci of residual tumor. In the remaining three, there was clinical and pathologic evidence of grossly disseminated carcinoma. Also in contrast to previous cases, all patients evidenced azotemia and proteinuria at the onset of the syndrome and ultimately uremia was a contributing cause of death. Coagulation profiles showed prolonged thrombin times and elevated fibrin degradation products in four instances and did not distinguish the patients with grossly metastatic disease from those with no tumor or only microscopic residua. Circulating immune complexes containing carcinoembryonic antigen were found in the patient with metastatic colon carcinoma. The syndrome was clinically identical whether or not grossly metastatic tumor was present, and it should not be attributed to advanced disease without definite clinical or pathologic evidence of a recurrence.
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PMID:Microangiopathic hemolytic anemia, thrombocytopenia, and renal failure in patients treated for adenocarcinoma. 728 73

A 39 year old man with 4 of the 5 cardinal features of the Laurence-Moon-Biedl syndrome (LMBS) had proteinuria and moderate renal failure. Excretory urography showed small cysts communicating with the dilated calyceal system. Renal biopsy showed diffuse mesangial sclerosis and cellular proliferation. Excretory urograms in 22 of 24 reported patients demonstrated similar findings. Review of renal pathology reports on 16 patients revealed either chronic glomerulonephritis or severe tubulo-interstitial disease with cysts or both in 8 of 9 who died from uremia and 2 of 7 who died from other causes. The abnormalities seen on excretory urography occur more frequently than 2 of the cardinal features, and as uremia is often the cause of death for these patients, renal disease should be considered a cardinal feature of LMBS.
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PMID:Renal disease-a sixth cardinal feature of the Laurence-Moon-Biedl syndrome. 729 73

At the Nephrology Department of the Hospital Infantil de Mexico, four cases of Alport's syndrome. with no relation among themselves, were studied between, June 1978 and November 1979. The diagnosis was based on the presence in the patients, of proteinuria and/or hematuria and in some of the relatives, a history of renal disease, deafness and a variable degree of renal failure; at the renal biopsy examined with electronic microscopy, there were findings compatible with Alport's disease in all four cases. Field studied were carried in the largest possible number of relatives for each family group the clinical viewpoint including measurement of blood pressure, examination of urine with reactive stripes to detect proteinuria and hematuria and audiologic examination. In the group, 130 subjects were studied out of a total of 237; 37% were found affected; 21% complaining of deafness; four female cases (19%) had not reach an uremic condition. From the second group 36 subjects were studied out of 109 members. Fifty per cent were found affected. Three cases had reached an uremic state (15%). Out of the third group with a total of 74 members, 34 cases were studied and 62% were found affected. Two female cases (12%) were complaining of uremia. The third group comprised 60 members and 19 of them were studied finding 13% affected with 2 cases of uremia. There were cases exclusively with renal or auditive involvement or both, at the same time. In our casuistics, most of the cases affected of the kidney or of the auditive apparatus were female patients; likewise, the most severely ill were females. Out of the 106 patients affected of the kidney, there were 11 with uremia and 8 were females. It was noticed that both males and females who were affected, had children of either sex with the same degree of affection, the same as other children with no changes at all; therefore, it is concluded that transmission is by dominant autosomal heredity.
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PMID:[Epidemiological study in 4 family units with Alport's syndrome]. 731 43


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