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)

Hypothyroidism, microscopic hematuria, and proteinuria developed in an 11-year-old girl. A renal biopsy specimen showed increased mesangial cells and matrix with focal glomerular basement membrane thickening. Three years later, a pronounced increase in proteinuria was detected. Elevated levels of antibody to thyroid microsomal antigen and thyroglobulin were found in the serum. A renal biopsy specimen showed a pronounced increase in mesangial cells and matrix with generalized glomerular basement membrane thickening. Electron microscopic studies demonstrated granular deposits in the capillary walls and mesangium. Immunofluorescent studies revealed granular deposits of IgG, IgM, and C3, primarily on the glomerular basement membrane. By indirect immunofluorescence, granular glomerular basement membrane and mesangial staining were detected with antibody specific for thyroglobulin and thyroid microsomal antigen. These observations suggest development of immune complex glomerulonephritis mediated by thyroid antigens.
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PMID:Immune complex glomerulonephritis mediated by thyroid antigens. 15 97

Four patients presented with nephrotic syndrome associated with hypothyroidism; none had thyroid antibodies. Hypothyroidism resolved on remission of nephrotic syndrome in two patients; thyroxine (T4) replacement was ineffective during periods of gross proteinuria in another, and the fourth had had normal thyroid function a year before presentation. Urinary T4 excretion was measured in ten further patients with proteinuria. It was detectable in the urine in five, who had significantly lower serum free T4 (8.5 [95% confidence interval 5.8-11.2] vs 13.9 [11.1-16.7] pmol/l; p less than 0.01) and free triiodothyronine (3.1 [2.2-4.0] vs 4.9 [3.8-6.0] pmol/l; p less than 0.01) concentrations than the five patients without detectable urinary T4.
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PMID:Can urinary thyroid hormone loss cause hypothyroidism? 167 46

Many lipoprotein abnormalities are seen in the untreated, hyperglycemic diabetic patient. The non-insulin-dependent diabetic (NIDDM) patient with mild fasting hyperglycemia commonly has mild hypertriglyceridemia due to overproduction of TG-rich lipoproteins in the liver, associated with decreased high-density lipoprotein (HDL) cholesterol levels. The more hyperglycemic untreated NIDDM and insulin-dependent diabetic (IDDM) patient have mild to moderate hypertriglyceridemia due to decreased adipose tissue and muscle lipoprotein lipase, (LPL) activity. These patients also have decreased HDL cholesterol levels associated with defective LPL catabolism of TG-rich lipoproteins. Treatment of diabetes with oral sulfonylureas or insulin corrects most of the hypertriglyceridemia and some of the decrease in HDL cholesterol. The abnormality in adipose tissue LPL activity corrects slowly over several months of therapy. The treated IDDM patient often has normal lipoprotein levels. The treated NIDDM patient may continue to have mild hypertriglyceridemia, increased intermediate-density lipoprotein levels, small dense low-density lipoproteins (LDL) with increased apoprotein B, and decreased HDL cholesterol levels. The central, abdominal distribution of adipose tissue in IDDM is associated with insulin resistance, hypertension, and the above lipoprotein abnormalities. Improvement in glucose control, in the absence of weight gain, leads to lower triglyceride and higher HDL cholesterol levels. In addition, the diabetic patient is prone to develop other defects that, in themselves, lead to hyperlipidemia, such as proteinuria, hypothyroidism, and hypertension, treated with thiazide diuretics and beta-adrenergic-blocking agents. When a diabetic patient independently inherits a common familial form of hypertriglyceridemia, he might develop the severe hypertriglyceridemia of the chylomicronemia syndrome.
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PMID:Pathophysiology of hyperlipidemia in diabetes mellitus. 171 Jul 39

Association between auto-immune dysthyroidism and glomerulonephritis is quite rare. The authors report 3 cases with proteinuria varying from 2.72 to 6.06 g/day and hypothyroidism. Nephrotic syndrome was found in 2 cases and thyroid auto-antibodies (microsomal and thyroglobulin) and circulating immun complexes (C.I.C.) in 1 case, complement fractions C3 and C4 were normal in all cases. Renal biopsy showed membranous glomerulonephritis in 2 cases and minimal lesions in the third case. Proteinuria disappeared with glucocorticoids and thyroxine in 1 case, with thyroxine alone in an other case and persisted in the third case with normal thyroid function.
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PMID:[Primary hypothyroidism and glomerular involvement]. 181 33

A 5-year-old mixed breed dog was presented with a history of depression and anorexia. Physical examination revealed a pharyngeal tumour and a neurological examination indicated the presence of a possible space-occupying lesion in the brain. Investigative procedures included a bloodsmear, impression smears and cytology of the pharyngeal tumour, haematology, chemical pathology, faecal analysis, urinalysis, electrocardiography, cerebrospinal fluid analysis, hormone assays and a computerised axial tomography scan. Results of these investigations revealed a round cell tumour in the pharynx, hypergammaglobulinaemia (34 g l-1), azotaemia (urea 8.6 mmol l-1 and creatinine 170 mumol l-1), hypoalbuminaemia (20 g l-1), proteinuria, sinus bradycardia (heart rate 60 beats per min), increased concentration of protein in the CSF (1.1 g l-1), hypoadrenocorticism (base line cortisol less than 55 nmol l-1) and hypothyroidism (T4 less than 13 nmol l-1). The computerised axial tomography scan revealed a brain tumour in the region of the hypophysis. The dog was euthanased and a post mortem examination confirmed the presence of a pharyngeal tumour with apparent direct extension of the tumour into the brain. Both tumours were confirmed histologically as mastocytomas.
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PMID:An expansile secondary hypophyseal mastocytoma in a dog. 251 66

Fifty-one women with type I diabetes who had normal thyroxine values before becoming pregnant were evaluated. Abnormalities of thyroid tests other than thyroxine were encountered in 26 women, of whom 8 developed a low serum thyroxine level, an elevated thyroid-stimulating hormone level, and a low insulin requirement in the second trimester subsequent to an increase in 24-hour urinary protein excretion to greater than 4 gm/24 hr. Thyroid replacement led to an increase in insulin requirement to levels appropriate for gestational age. It is concluded that the woman with type I diabetes who develops proteinuria greater than 4 gm/24 hr during gestation is at risk for the development of de novo hypothyroidism during pregnancy, evidenced by a low serum thyroxine level, an elevated thyroid-stimulating hormone level, and a drop in insulin requirement.
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PMID:De novo clinical hypothyroidism in pregnancies complicated by type I diabetes, subclinical hypothyroidism, and proteinuria: a new syndrome. 304 13

The thyroid function of 13 patients with proteinuria and normal serum creatinine level (Group 1) and 15 patients with proteinuria and increased creatinine level (Group 2) was investigated. The daily urinary T41- and T3 excretion was much higher in Group 1 patients than in Group 2 patients (37.1 +/- 25.9 nmol T4 vs 17.5 +/- 8.7 nmol T4, 3.3 +/- 1.6 nmol T3 vs 1.1 +/- 0.8 nmol T3, respectively) and correlated in both groups with the protein loss. None of the patients suffered from hypothyroidism as a consequence of this hormone loss. Although the mean serum T4-, T3-, FT4-, FT3-, TBG- and TBPA concentrations in both groups of patients were within the normal range, the urinary hormone loss appeared to influence these values considerably. It was striking that the rT3 concentration in the patients with the highest hormone loss was frequently less than 0.08 nmol/l, the lower limit of detectability. The basal TSH levels in serum of the nephrotic patients were similar to those of normal individuals. The thyroid function of patients with proteinuria accompanied by retention of creatinine due to renal failure was more difficult to assess because different pathological mechanisms may exert their influence on the thyroidal hormone secretion as well as on the peripheral hormone metabolism.
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PMID:Thyroid function in patients with proteinuria and normal or increased serum creatinine concentration. 640 73

A 54-year-old woman who had proteinuria due to stage II membranous nephropathy is reported. She was treated with indomethacin for proteinuria and developed drug-induced hepatitis four months later. Liver dysfunction gradually recovered, but hormonal studies revealed abrupt fall of T3 and T4 and concomitant elevation of TSH levels within a month. Pathological findings of thyroid specimen and positive antithyroglobulin and antimicrosomal antibodies were compatible to chronic thyroiditis. In the second renal biopsy, glomerular deposits of thyroglobulin, thyroid microsomal antigens and IgG were demonstrated by immunofluorescence. Therefore, membranous nephropathy in this patient is presumed to be caused by immune complexes mediated by thyroid constituents. We believe that this is a precious case because continuous changes in T3, T4 and TSH were followed in a course of chronic thyroiditis, especially in the stage of progress to hypothyroidism, and the chronic thyroiditis was shown to be involved in the membranous nephropathy.
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PMID:A case of membranous nephropathy associated with thyroid antigens. 706 40

Hypothyroidism diminishes proteinuria and prolongs survival in several immune models of progressive renal failure. In the well-characterized non-immune model of 5/6 nephrectomy we studied the effects of thyroidectomy (Tx) on the development of proteinuria and glomerulosclerosis (GS). Hypothyroidism was confirmed by lower values of thyroxine in Tx rats compared to sham Tx rats at 9 weeks (12.6 +/- 6.7 nmol/l Tx versus 37.7 +/- 10.8 nmol/l sham Tx) and 12 weeks after operation (7.2 +/- 4.9 nmol/l Tx versus 14.4 +/- 4.1 nmol/l sham Tx). Tx resulted in a reduction in mean arterial blood pressure and proteinuria and a lower incidence of GS (4.2 +/- 3.1% Tx versus 17.1 +/- 10.0% sham Tx) 12 weeks after nephrectomy, along with a decrease in food intake (104 +/- 13 g/week Tx versus 138 +/- 10 g/week sham Tx). In the same experiment a third group of sham Tx rats was pair fed to the Tx rats, resulting in values similar to those of Tx rats for proteinuria and the incidence of GS (6.0 +/- 4.9% pair fed sham Tx). Thyroxine levels at 9 and 12 weeks were comparable to those in sham Tx rats fed ad libitum. No association was found between the incidence of GS and glomerular volume. Studies of the inulin clearance in a second set of experiments showed that glomerular filtration rate and renal plasma flow are lower in hypothyroid rats compared to sham Tx rats. We conclude that hypothyroidism has a renal protective effect due to a decrease in food intake resulting in alterations in renal haemodynamics.
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PMID:Hypothyroidism retards progressive glomerulosclerosis in the rat by a reduction in food intake. 815 3

A case of severe hypothyroidism in a 51-year old male is presented. The patient was especially complaining of weakness, stiffness and moderate pain in the proximal muscle groups together with rhinorrhea and nasal stenosis. Because of severely elevated S-creatine-kinase combined with reduced creatinine clearance and proteinuria, polymyositis with secondary glomerulopathy was suspected. Meanwhile, biopsies from skin, muscle, and kidney were normal. All symptoms disappeared 3 months after thyroid replacement therapy was initiated. S-TSH should be considered when evaluating patients with renal impairment of unknown etiology.
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PMID:Severe hypothyroidism masquerading as renal impairment. 877 59


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