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 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

A case of systemic lupus erythematosus (SLE) complicated with hypopituitarism after steroid pulse therapy is reported. A 46-years-old-female with a history of SLE starting in 1975 was admitted to our hospital in February 1991 for lupus nephritis. Steroid pulse therapy, 1000 mg methyl-prednisolone for 3 successive days as one therapy unit, was administered. Proteinuria improved remarkably, however, general fatigue and headache appeared 2 weeks after initiation of therapy. Endocrinological examination revealed hypopituitarism including the levels of TSH, FSH, GH and ACTH. The secretion of FSH and LH gradually improved after replacement therapy of dried thyroid. MRI examination of the brain revealed an empty sella. It is known that pituitary tumor, cerebrovascular accident and autoimmune lymphocytic hypophysitis cause hypopituitarism. In this case, it is unlikely that the pulse therapy may be responsible for the infarction of the anterior pituitary artery furthermore, there has been no articles describing such incidence after steroid pulse therapy. This case may be indicative of a very rare case in which the empty sella might have been exacerbated by the pulse therapy in the causation of hypopituitarism.
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PMID:[Hypopituitarism associated with empty sella after steroid pulse therapy in a patient with SLE]. 814 29

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

POEMS syndrome is a multisystem disorder with signs such as peripheral neuropathy, organomegaly, endocrinopathy, monoclonal protein, skin lesions, papilledema, and increased cerebrospinal fluid proteins, which can also evolve with renal and cardiac affection. It is considered a result of a plasma cell cyscrasia with the production of a monoclonal protein. A 46-year old man was seen as an outpatient referring progressive weakness of legs and arms, fever, impotence, inguinal and cervical lymphadenopathies, peripheral edema, hepatomegaly and skin hyperpigmentation. In laboratory test, platelet count was between 528 x 10(9)/L and 599 x 10(9)/L, creatinine clearance 27.2 ml/min, proteinuria 0.8 g/dl, IgA 455 mg/dl, T3 30 ng/100 ml, T4 2.6 vg/dl, T4F 0.5 ng/dl, TSH 12.4 vU/ml; testosterone 1.56 ng/ml. The electromyography showed a mixed sensitive-motor pattern. On the pelvis radiography, an osteosclerotic lesion on the left sacroiliac joint was identified. Bone biopsy of the site of the sclerotic lesion revealed plasma cell dyscrasia. The patient was treated with diuretics, digitalis and prednisone. Diagnosis of this disorder is difficult because of the multipathology it is necessary to establish differential diagnosis.
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PMID:[POEMS syndrome. Report of a case]. 1042 26

Hashimoto's thyroiditis and membranous nephropathy are believed to be mediated by immune mechanisms. A 12 year-old patient is reported who presented with fatigue, dislike of cold, pallor and growth retardation. Initial laboratory assessment showed moderate proteinuria and impaired renal function (serum creatinine 2.3 mg/dl), and hypothyroidism due to autoimmune thyroiditis. Light, immunofluorescence and electron microscopy of the renal biopsy showed membranous nephropathy. The patient recovered from nephropathy after substitution of thyroid hormone and therapy with prednisone. Megalin can be envisaged as a potential pathogenetic link between the two disease entities. The glycoprotein megalin is expressed on thyroid cells in a TSH-dependent manner and may have a crucial role in the immunopathogenesis of glomerular injury in membranous nephropathy. For similar cases, we want to encourage colleagues to consider this hypothesis and to examine blood and renal biopsy specimens for the presence of megalin and antibodies against it.
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PMID:Autoimmune thyroiditis in association with membranous nephropathy. 1496 28

In 2002, a 38-year-old woman was referred to the department of dermatological sciences for the evaluation of erythematous-infiltrated lesions with prominent purpuric and erosive components distributed on her face, upper chest, and extensor surfaces of the limbs, which developed over a 3-month period. In 1997 the patient suffered from polyarthralgia (proximal interphalangeal,knee, wrist, and metacarpophalangeal joints) associated with morning stiffness. In 1999 she was admitted to a psychiatric unit for depression with episodes of lipothymia. In the same year, since she developed diffuse and persistent urticarial manifestations with angioedema and livedo reticularis of the limbs in association with anticardiolipin antibodies, vasculitis was proposed. Upon examination, erythematous-infiltrated and erosive lesions in association with serohemorrhagic crusts were present on the face,neck, chest, upper trunk, and extensor surfaces of the upper limbs and thighs (Figures 1-3). Telangiectasias were especially evident on the cheeks, where prominent edema conferred her face a moon-like appearance (Figure 1). Laboratory investigations disclosed microcytic anemia, elevated erythrocyte sedimentation rate, proteinuria (30 mg/dL), positive antinuclear antibodies (1:80) with diffuse fluorescence pattern, lowered complement levels (C3: 31 mg/dL, C4: 3 mg/dL), circulating immunocomplexes binding Clq, and high titers of anti-TSH receptor antibodies. Indirect immunofluorescence was negative for the detection of anti-basement membrane zone antibodies. Histological examination of the lesional skin of the shoulder documented epidermal atrophy, marked vacuolar degeneration of the basal cell layer, colloid bodies, and a perivascular lymphohistiocytic infiltration of the upper and deep dermis (Figure 4). Direct immunofluorescence performed on affected skin showed junctional granular deposition of IgG, C3,and Clq in association with perivascular C3 and Clq deposits in the upper dermis; direct immunofluorescence on sun-protected,non-lesional skin showed similar immunological deposition both at the basement membrane zone and in the perivascular dermis.Based upon the clinical, histologic, and immunopathologic findings, we proposed the diagnosis of systemic lupus erythematosus with maculopapular and erosive skin lesions. The patient was treated with methylprednisolone IV (pulse therapy, 250 mg) tapered over 10 days and later continued p.o. After a few weeks, significant improvement of cutaneous manifestations was noted.
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PMID:Systemic lupus erythematosus with unusual maculopapular and erosive cutaneous lesions. 1536 71

Genetic inactivation of ClC-5, a voltage-gated chloride channel prominently expressed in the kidney, leads to proteinuria because of defective apical endocytosis in proximal tubular cells. Because thyroid hormone secretion depends on apical endocytosis of thyroglobulin (Tg), we investigated whether ClC-5 is expressed in the thyroid and affects its function, using Clcn5-deficient knockout (KO) mice. We found that ClC-5 is highly expressed in wild-type mouse thyroid ( approximately 40% of mRNA kidney level). The protein was immunolocalized at the apical pole of thyrocytes. In Percoll gradients, ClC-5 overlapped with plasma membrane and early endosome markers, but best codistributed with the late endosomal marker, Rab7. ClC-5 KO mice were euthyroid (normal T4 and TSH serum levels) but developed a goiter with parallel iodine and Tg accumulation (i.e. normal Tg iodination level). When comparing ClC-5 KO with wild-type mice, thyroid 125I uptake after 1 h was doubled, incorporation into Tg was decreased by approximately 2-fold, so that trichloroacetic acid-soluble 125I increased approximately 4-fold. Enhanced 125I- efflux upon perchlorate and presence of 125I-Tg as autoradiographic rings at follicle periphery demonstrated delayed iodide organification. Endocytic trafficking of 125I-Tg toward lysosomes was not inhibited. Expression of pendrin, an I-/Cl- exchanger involved in apical iodide efflux, was selectively decreased by 60% in KO mice at mRNA and protein levels. Thus, ClC-5 is well expressed in the thyroid but is not critical for apical endocytosis, contrary to the kidney. Instead, the goiter associated with ClC-5 KO results from impaired rate of apical iodide efflux by down-regulation of pendrin expression.
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PMID:The loss of the chloride channel, ClC-5, delays apical iodide efflux and induces a euthyroid goiter in the mouse thyroid gland. 1630 76

Immunoglobulin A (IgA) nephropathy can rarely be associated with thyroid disease. We present a case of a young lady with nephrotic range proteinuria, microscopic hematuria, a creatinine clearance of 67 ml/min, biopsy proven IgA nephropathy, in whom hypercholesterolemia persisted after immunosuppressive therapy induced remission of glomerulonephritis. Fluvastatin was given but rhabdomyolysis developed. Unexpectedly, CK remained elevated following discontinuation of fluvastatin. Secondary amenorrhoea prompted endocrine work-up and hypothyroidism was diagnosed. Cholesterol, CK and TSH values became normal within 3 months on L-thyroxin therapy. The literature of the association of glomerular diseases and thyroid illness is reviewed. We would like to draw the attention to the possible association of glomerular pathologies and thyroid diseases and the importance of ruling out hypothyroidism and measuring CK level before starting statin therapy.
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PMID:Association of IgA nephropathy, hypothyroidism and hypercholesterolemia. 1635 38

Endocytosis is a distinctive property of all eukaryotic cells. Polarized cells face two different worlds by membranes of distinct composition: the basolateral membrane is exposed to the constant internal medium, whereas the apical membrane is exposed to variable environments. Endocytosis on both aspects also depends on different machineries. This short review illustrates the molecular basis and physiopathological implications of apical endocytosis. In a cultured epithelial cell line, Src selectively triggers apical macropinocytosis by activating the actin cytocortex via signalling membrane lipids generated by an amplification cascade involving phosphoinositide 3-kinase, phospholipase C and phospholipase D. Several actors of Src response are also activated by enteroinvasive bacteria, to trigger their entry into enterocytes. In the thyroid gland, the rates of thyroglobulin apical micropinocytosis and transfer to lysosomes determine the level of thyroid hormone production, by controlling the encounter of the prohormone with converting hydrolases. TSH selectively promotes the encounter, by inducing the expression of rate-limiting catalysts, the small GTPases Rab5 and Rab7, and of their exchange factor(s). This induction is constitutive in autonomous adenomas. In kidney proximal tubular cells, apical receptor-mediated endocytosis ensures full recapture of ultrafiltrated proteins. Inactivating mutations of the endosomal chloride channel, ClC-5, that are responsible for Dent's disease, cause a loss of surface receptors leading to proteinuria. These examples illustrate how three levels of regulation of apical endocytosis, namely the mode of entry, the rate of vesicular trafficking and the subcellular addressing account for a variety of human diseases.
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PMID:[Apical endocytosis: molecular controls and physiopathologic implications]. 1639 73


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