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)

Patients with nephrotic syndrome have low blood levels of 25 hydroxyvitamin D (25-OH-D) most probably because of losses in urine, and a vitamin D-deficient state may ensue. The biological consequences of this phenomenon on target organs of vitamin D are not known. This study evaluates one of these target organs, the bone. Because renal failure is associated with bone disease, we studied six patients with nephrotic syndrome and normal renal function. The glomerular filtration rate was 113+/-2.1 (SE) ml/min; serum albumin, 2.3+/-27 g/dl; and proteinuria ranged between 3.5 and 14.7 g/24 h. Blood levels of 25-OH-D, total and ionized calcium and carboxy-terminal fragment of immunoreactive parathyroid hormone were measured, and morphometric analysis of bone histology was made in iliac crest biopsies obtained after double tetracycline labeling. Blood 25-OH-D was low in all patients (3.2-5.1 ng/ml; normal, 21.8+/-2.3 ng/ml). Blood levels of both total (8.1+/-0.12 mg/dl) and ionized (3.8+/-0.21 mg/dl) calcium were lower than normal and three patients had true hypocalcemia. Blood immuno-reactive parathyroid hormone levels were elevated in all. Volumetric density of osteoid was significantly increased in three out of six patients and the fraction of mineralizing osteoid seams was decreased in all. Evidence for an increase in active lacunae (bone-osteoclast interface) occurred in three out of six patients and in inactive (Howship's lacunae) bone resorption in six out of six. The data indicate that the loss of 25-OH-D in urine of patients with nephrotic syndrome and normal renal function may result in a decrease of blood levels of ionized calcium, secondary hyperparathyroidism and enhanced bone resorption. In addition, the vitamin D-deficient state causes osteomalacia as evidenced by defective mineralization and increased osteoid volume.
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PMID:Osteomalacia and hyperparathyroid bone disease in patients with nephrotic syndrome. 42 68

Tubular proteinuria is generally accepted as the critical effect following long-term, low-level exposure to cadmium as seen in an industrial environment. This effect may not be of immediate importance to the health of the individual, but the significance, in terms of long-term morbidity and mortality, of the renal tubular defect of which it is an indicator is not fully understood, and certain sequelae may have remained unrecognized due to inadequate follow-up.Follow-up studies have been performed in nine of 12 workers who were initially investigated in 1962. In six of the men exposures ranged from 28 to 45 years to cadmium sulfide dust and for shorter periods in the earlier years to cadmium oxide fume and dust. These six men had tubular proteinuria when first seen, and this has persisted in the five survivors. All six men had hypercalciuria, and two of them became recurrent stone formers. One man whose urinary calcium excretion later fell to a low level more recently developed vitamin D resistant osteomalacia. In addition, each of the six men had exhibited some, but not all, of a variety of biochemical abnormalities related to other proximal renal tubular defects, and the worker who developed osteomalacia had additional evidence of a distal tubular defect. The five survivors also have evidence of slowly progressive deterioration in glomerular function.Follow-up of this small group has shown that renal tubular dysfunction in cadmium workers may continue symptom-free for long intervals, but in a proportion of cases serious clinical effects may develop after a number of years.
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PMID:Renal tubular dysfunction and abnormalities of calcium metabolism in cadmium workers. 48 32

Two patients with intractable massive proteinuria and uremia were followed and treated with standard mecial 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. Table I: Possible advantages of medical nephrectomy. 1. Reversal of hypotension and shock 2. Ability to perform hemodialysis 3. No anesthesia or surgical risk 4. No angiography related complications 5. Preservation of endocrine function of kidney. Possible advantages of medical nephrectomy (Table I), are: 1) Correction of proteinuria and hypotension; 2) Ability to perform hemodialysis; 3) No anesthesia or surgical risk; 4) No angiography related complications; and 5) Preservation of remaining endocrine function of the kidney, including erythropoietic and vitamin D action. The ideal agent should be non-toxic to other organs and produce selective renal ablation. Obviously mercury is not the ideal agent, although in these cases it did not produce observable side effects. It appears that this agent should be used with caution and only in patients with irreversible renal failure.
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PMID:Medical nephrectomy. The use of metallic salts for the control of massive proteinuria in the nephrotic syndrome. 95 62

Relative hypocalciuria has been reported in women with preeclampsia. However, there has been no systematic explanation for this finding. We measured serum and urinary calcium and serum calciotropic hormones in third trimester women with preeclampsia (n = 12, gestational hypertension and proteinuria) and with normotensive pregnancies (n = 24) to try to explain these changes. We confirmed that the women with preeclampsia have a relative hypocalciuria (2.9 +/- 0.7 vs. 6.5 +/- 0.2 mmol/day, P less than 0.01). Preeclamptic women also had lower serum ionized calcium than normotensive third trimester pregnant women (1.20 +/- 0.01 vs. 1.26 +/- 0.01 mmol/L, P less than 0.02). Intact PTH levels were significantly higher in preeclamptic women (29.9 +/- 4.3 vs. 15.4 +/- 1.3 ng/L, P less than 0.01) and a significant inverse relationship was observed between PTH and both urine calcium (r = -0.60, P less than 0.0001) and serum ionized calcium (r = -0.36, P less than 0.05). We measured vitamin D metabolites in a subgroup of both normotensive and preeclamptics. Preeclamptic and normotensive pregnant women had equivalent levels of 25-hydroxyvitamin D [25(OH)D]; however, preeclamptics had significantly lower 1,25-dihydroxyvitamin D [1,25-(OH)2D] levels (172.1 +/- 18.5 vs. 219.6 +/- 12.7 pmol/L, P less than 0.05). Lower 1,25-(OH)2D may contribute to suboptimal intestinal absorption of calcium during a time of increased calcium demand resulting in lower ionized calcium, increased PTH, and hypocalciuria in preeclampsia. Abnormalities in calcium homeostasis may contribute to the increased vascular sensitivity documented in preeclampsia.
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PMID:Lower serum ionized calcium and abnormal calciotropic hormone levels in preeclampsia. 159 91

The murine strain MRL/l spontaneously develops a systemic lupus erythematosus (SLE)-like syndrome. An increased number of T cells and polyclonal T helper cell activity has been described in these mice suggesting a potential role for 1,25-dihydroxyvitamin-D3 [1,25-D3], an antiproliferative hormone selecting the T-helper lymphocyte subset. One month old MRL/l mice were submitted or not to 1,25-D3 0.1 microgram for 4 weeks, then 0.15 microgram given i.p. every other day for 18 weeks while maintained on a low calcium chow. Dermatologic lesions, i.e. alopecia, necrosis of the ear and scab formation, were completely inhibited by 1,25-D3 therapy. By 20 weeks, all mice had developed proteinuria. However, the degree of proteinuria was somewhat reduced in treated mice as assessed by urine protein/creatine ratios (less than 4 vs greater than 4 in treated vs untreated mice respectively). Moreover, a trend for a reduction in serum titers for anti-ssDNA antibodies was observed at 18 weeks. The active vitamin D metabolite had no effect on the development of the generalized lymphoid hyperplasia. Hypercalcemia developed when 1,25-D3 was increased to 0.15 microgram (2.62 +/- 0.12 vs 1.97 +/- 0.07 mmol/l, treated vs untreated mice respectively). These results suggest a beneficial role of 1,25-D3 in the prevention or attenuation of some manifestations of murine SLE, a model sharing many immunologic features with human SLE.
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PMID:1,25-Dihydroxyvitamin D3 attenuates the expression of experimental murine lupus of MRL/l mice. 161 11

Nephrotic syndrome (NS) is commonly associated with vitamin D deficiency. Urinary losses of the protein-bound intermediary metabolite of this vitamin is thought to contribute to the deficiency state. The role of possible changes, if any, of vitamin D absorption has not been investigated previously in NS. We determined intestinal absorption of vitamin D3 as well as plasma concentration and urinary excretion of 25-hydroxyvitamin D3 in rats with puromycin aminonucleoside-induced NS. In vivo recirculating perfusion technique was employed at 100 and 600 nM perfusate concentrations. The results were compared with those obtained in animals receiving placebo injections provided with either free access to food (normal controls) or those pair-fed with their NS counterparts (pair-fed group). The NS group showed heavy proteinuria and hypoalbuminemia. In addition, the NS group exhibited marked urinary losses and significantly reduced plasma concentration of 25-hydroxyvitamin D. The rate of vitamin D3 absorption (given as nmol/100 cm/min) at 100 nM perfusate concentration in the NS group (0.161 +/- 0.029) was not significantly different from those obtained in the pair-fed group (0.202 +/- 0.058) and the normal control group (0.143 +/- 0.053). Likewise, no significant difference was found in the rats of vitamin D absorption at 600 nM concentration among the NS (1.073 +/- 0.383), pair-fed (0.955 +/- 0.229), and normal control (0.756 +/- 0.314) groups. Accordingly, intestinal absorption of vitamin D appears to be unaffected by the presence of experimental NS and as such the associated vitamin D deficiency can be managed by enteral supplementation.
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PMID:Vitamin D absorption, plasma concentration and urinary excretion of 25-hydroxyvitamin D in nephrotic syndrome. 199 Apr 9

Zinc content of serum, hair and erythrocytes, urinary zinc excretion, zinc clearance (CZn) and the ratio of CZn to creatinine clearance (CCr) (CZn/CCr) were measured in 32 children aged between 2.1 and 14.4 years suffering from idiopathic nephrotic syndrome (INS) without renal failure (CCr greater than 70 ml/min 1.73 m2 body surface area). Nineteen subjects had proteinuria and the remaining 13 were in remission. All children received calcium and vitamin D supplementation while on steroid therapy. There was high dietary zinc and protein intake. The results were compared with those obtained from 19 healthy subjects (aged 2-14 years). Zinc concentration in serum, erythrocytes and urine were measured by a colourimetric method. Proton induced X-ray emission was used to determine zinc content in hair. In patients both with and without proteinuria, the mean contents of serum, hair and erythrocytes were significantly lower than in the control group. The urinary zinc excretion, CZn and CZn/CCr in INS children were significantly higher than in the control group. A positive correlation was found between urinary zinc and protein excretion. In spite of high dietary zinc intake and normal intestinal absorption, children with INS had a zinc deficiency. This was probably caused by an increased urinary zinc loss.
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PMID:Impaired zinc metabolic status in children affected by idiopathic nephrotic syndrome. 233 16

Two patients, one with myeloma (Patient 1) and the other with probable chronic lymphocytic leukemia (Patient 2), had reduced renal tubular phosphate reabsorption in the absence of hyperparathyroidism together with other features of the Fanconi syndrome, as consequences of the nephropathy associated with light-chain proteinuria. Both patients had hypophosphatemic osteomalacia, demonstrated for the first time in this condition by iliac bone histomorphometry after in vivo double tetracycline labeling, despite absence of bone pain or Looser zones. Neither patient was vitamin D-depleted, but plasma calcitriol level was normal in Patient 1 and low in Patient 2; only the latter patient had severe muscle weakness. Complete histologic correction of osteomalacia was achieved by treatment in accordance with the biochemical defects--oral phosphate therapy alone in Patient 1 and combined with calcitriol in Patient 2. Both patients are now symptom-free, five and three years after the initial diagnosis of bone disease and hematogenous malignancy. Thirteen previous instances of the same form of osteomalacia were reviewed; in most cases, the Fanconi syndrome developed before its probable cause became apparent. The Fanconi syndrome has also been reported in two cases of osteomalacia due to mesenchymal tumor, but not in osteomalacia associated with prostatic carcinoma. Light-chain nephropathy and consequent renal tubular dysfunction appears to be a third form of oncogenous osteomalacia.
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PMID:Hypophosphatemic osteomalacia and adult Fanconi syndrome due to light-chain nephropathy. Another form of oncogenous osteomalacia. 310 97

Recent studies indicate that serum levels of osteocalcin, a 49-aminoacid bone matrix protein, are a biochemical marker of bone formation. In order to study bone metabolism in diabetes mellitus, in 28 patients with Type 1 (insulin-dependent) diabetes mellitus, in 38 patients with Type 2 (non-insulin-dependent) diabetes mellitus and two control groups, matched for Type 1 and Type 2 diabetic patients, respectively, serum levels of osteocalcin, parathyroid hormone and 25 hydroxy vitamin D were measured by radioimmunoassay. Whereas in Type 1 diabetic patients and control subjects serum levels of osteocalcin and 25 hydroxy vitamin D were not statistically different, serum osteocalcin and 25 hydroxy vitamin D levels were significantly decreased in Type 2 diabetic patients when compared with corresponding control subjects (p less than 0.03 and p less than 0.001, respectively). Independent of the type of diabetes, serum parathyroid hormone levels were comparable in diabetic patients and matched control subjects. Serum osteocalcin levels were significantly lower in Type 1 diabetic patients with retinopathy and/or proteinuria than in Type 1 diabetic patients without microangiopathy (p less than 0.05). Whereas serum parathyroid hormone levels in Type 2 diabetic patients with retinopathy and/or proteinuria were significantly increased (p less than 0.02), 25 hydroxy vitamin D levels were decreased (p less than 0.02) when compared with Type 2 diabetic patients without microangiopathy. Our data give evidence of a vitamin D deficiency and a decreased bone formation in patients with Type 2 diabetes mellitus. In Type 1 diabetes mellitus bone formation as reflected by serum osteocalcin levels is influenced by the presence or absence of microangiopathic complications.
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PMID:Serum osteocalcin levels in diabetes mellitus: analysis of the type of diabetes and microvascular complications. 326 86

A 44-year-old Chinese male with a 7-year history of diabetes developed spontaneous fractures affecting the femur and distal tibia and fibula within a period of 4 months. Spontaneous rib fractures were also present. There was additional evidence of extensive tissue damage with retinopathy, proteinuria, necrobiosis lipoidica diabeticorum, peripheral neuropathy and autonomic neuropathy. Investigation confirmed the presence of generalised osteoporosis and showed no evidence of other metabolic bone disease or abnormal vitamin D metabolism. Mild hypogonadism was also present and investigation suggested a disturbance of hypothalamic-pituitary control of gonadal function. It is suggested that the severe generalised osteoporosis resulted from poorly controlled diabetes with a possible additional contribution from androgen deficiency secondary to the diabetes.
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PMID:Fractures due to severe generalised osteoporosis in a 44-year-old male with diabetes mellitus. 277 56


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