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)

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

We report a case of HAM/TSP presenting with short stature, mental retardation, skin eruptions, uterine and ovarian hypogenesis and nephropathy. Skin erythema was noted since from the age of three years old and spasticity of lower extremities from elementary school age. Serum calcium level showed 4.1 mEq/l. Recombinant human PTH infusion resulted in no response of phosphate excretion. The persistent proteinuria prompted renal needle biopsy, which revealed IgA and C1q deposits in glomerular mesangium. A diagnosis of pseudohypoparathyroidism and IgA nephropathy was entertained. This patient with pseudohypoparathyroidism who has a deficient immune system was seized with the early onset of HAM/TSP and IgA nephropathy.
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PMID:A case of HTLV-I-associated myelopathy with IgA nephropathy and pseudohypoparathyroidism type 1. 179 21

Patients with idiopathic recurrent calcium nephrolithiasis (n = 57) and controls (n = 16) were investigated regarding the relationship between renal phosphate handling, other renal tubular functions and calcium metabolism. Incomplete renal tubular acidosis (RTA) was disclosed in 13 patients. RTA patients together with stone formers with normal renal acidification capacity (SF) exhibited low values for serum phosphate and renal threshold phosphate concentration (TmP/GFR) compared with controls. TmP/GFR was lower in RTA patients than in stone formers with normal renal acidification. Hypercalciuria of the absorptive type with normal serum PTH and urinary cAMP concentrations was a common finding in both stone patient groups, whereas no patient displayed unequivocal evidence of parathyroid hyperfunction. Fractional excretion of sodium was raised in both SF and RTA patients compared with controls. There was a positive relationship between the fractional excretion of phosphate and sodium in all subjects as a group. TmP/GFR was negatively correlated to fractional excretion of sodium. Twenty-three percent of RTA patients and 8% of SF displayed tubular proteinuria which often was associated with low TmP/GFR levels and enhanced natriuresis. It is concluded that a defective renal tubular phosphate handling is common in calcium stone formers and often associated with signs of other tubular dysfunctions. The altered phosphate handling seems to be unrelated to hypercalciuria.
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PMID:Phosphate metabolism in renal stone formers. (II): Relation to renal tubular functions and calcium metabolism. 627 2

Bone histology and its relationship with calcium metabolism was evaluated in adult patients with nephrotic syndrome: 29 had normal renal function (GFR 103 +/- 4 ml/min/1.73 m2) (group 1) and 20 had renal insufficiency (GFR 31 +/- 4 ml/min/1.73 m2) (group 2). In group 1, serum PTH, 1.25-HCC and 24.25-HCC levels were normal, while 25-HCC values were reduced. Bone histology was normal in 76% of the patients, while 17% had isolated osteomalacia and 7% an associated bone resorption. Group 2 showed a higher incidence of bone resorption when compared with a matched group of patients with renal failure and no proteinuria (40% vs. 13%) and a comparable frequency of isolated mineralization defect (25% vs. 34%). PTH levels were definitely increased and serum total calcium and all the vitamin D metabolites were reduced. A significant correlation between the apparent duration of the disease and the severity of osteodystrophy was found only in group 2. In conclusion, no constant derangement of calcium metabolism and bone histology is evident in patients with nephrotic syndrome and normal renal function, while patients with persistent proteinuria are at high risk of osteodystrophy even in the early phases of renal failure.
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PMID:Bone histology and calcium metabolism in patients with nephrotic syndrome and normal or reduced renal function. 673 66

Patients with the nephrotic syndrome and normal renal function have low levels of 25(OH)D in serum presumably due to the loss of this metabolite in the urine. Osteomalacia and hyperparathyroidism have been recently reported to occur as a consequence of those low levels of 25-hydroxyvitamin D (25OHD). We studied six patients (aged 26-52 yr) with the nephrotic syndrome (mean duration, 6.7 yr; range, 2-12 yr) and normal renal function, and evaluated their calcium, phosphorus, PTH, and vitamin D metabolite levels. Bone biopsies were obtained in all patients. The creatinine clearance ranged from 83-134 ml/min . 1.73 m2 of body surface, serum albumin was 2.65 +/- 0.42 (+/- SD) g/100 ml, and proteinuria ranged from 3.5-13.2 g/24 h. All patients had normal serum magnesium, phosphorus, ionized calcium, and alkaline phosphatase (total and bone fraction), and normal roentgenographic metabolic bone survey. Serum PTH, measured by the carboxy-terminal RIA, was 5.1 +/- 2.3 mu leq/ml (normal, 2-10), serum 250HD was 8.8 +/- 4.0 ng/ml (normal, 15-30), and 1,25-dihydroxyvitamin D3 was 38 +/- 25 pg/ml (normal, 17-58). Serum vitamin D-binding protein was 420 +/- 42 micrograms/ml (normal, 400-800). The histological appearance of bone biopsies obtained in these patients was not different from that in a group of sex- and age-matched controls. Specifically, there was no increase in the volume of osteoid (unmineralized bone), the percentage of trabecular surface covered by osteoid, or the number of osteoclasts. The cellular rate of mineralization was normal in all six patients. Thus, these data indicate that low serum levels of 250HD in patients with the nephrotic syndrome and normal renal function do not necessarily result in the development of osteomalacia and/or hyperparathyroidism.
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PMID:Absence of metabolic bone disease in adult patients with the nephrotic syndrome and normal renal function. 682 51

In the present study calcium and vitamin D metabolism was studied in fifty patients with daily urinary protein excretion exceeding 3 g/24 hours. A positive correlation was seen between serum albumin and ionized calcium concentration (r = 0.51, p < 0.001). All patients with normal renal function had their intact PTH within normal range, though seven of these 16 had serum ionized calcium below the lower margin of the reference range. The mean serum albumin was significantly lower in the seven patients with low serum ionized calcium when compared with those with serum ionized calcium above the lower normal margin (19 g/l vs. 30 g/l, respectively, p < 0.001), but there was no difference in plasma intact PTH (3.7 +/- 1.3 pmol/l vs. 3.1 +/- 0.7 pmol/l, p = 0.21, ns.). Serum 25OHD3 correlated negatively with the degree of proteinuria (r = -0.50, p < 0.001) and positively with serum albumin (r = 0.66, p < 0.001). Serum 1,25(OH)2D3 was related to serum 25OHD3 (r = 0.39, p < 0.01), but its association with serum phosphate, PTH, the degree of proteinuria and renal function did not reach statistical significance. In conclusion, a significant correlation between serum ionized calcium and albumin was observed, and in hypoalbuminemia hypocalcemia did not induce PTH response of expected magnitude. In patients with marked hypoalbuminemia a low measured ionized calcium does not have the same clinical impact as it would have in normoalbuminemia and it has to be interpreted cautiously. Secondly, abnormal regulation of 1,25(OH)2D3, and in particular its dependency on 25OHD3, was observed in patients with heavy proteinuria.
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PMID:Calcium and vitamin D homeostasis in patients with heavy proteinuria. 805 Feb 9

We studied the effect of induced hyper- and hypocalcemia on parathyroid function and renal handling of phosphate in healthy subjects (n = 10) and in patients with heavy proteinuria, mean 5.6 +/- 1.9 g/24 hours (n = 5). We used calcium and citrate clamp techniques. Hypercalcemia was rapidly induced by calcium infusion and maintained for 120 min, and correspondingly, hypocalcemia by citrate infusion. The suppression of intact PTH secretion during calcium clamp was similar (to the level of < or = 0.8 pmol/l) in both groups. The response of the parathyroid glands to hypocalcemia was similar in normal subjects and proteinuric patients. Both groups showed a peak of PTH secretion at 10 min, 18.9 +/- 6.7 pmol/l in healthy subjects and 20.4 +/- 7.4 pmol/l in patients. The peak levels were 4.8-7.2 times and 4.0-6.7 times the baseline level, respectively. Thereafter the plasma PTH concentration declined to a fairly constant steady-state level (twice the baseline level) in spite of maintained hypocalcemia. The area under the curve of the plasma concentrations of intact PTH at various times (AUC0-120) was 890 +/- 324 pmol/l/min in normal subjects and 989 +/- 331 pmol/l/min in proteinuric patients, the difference between the groups being again not significant. The renal threshold phosphate concentration (TmPO4/GFR) increased during calcium infusion and decreased during citrate infusion in both groups. During recovery from hypocalcemia PTH levels were lower than during hypocalcemic induction at corresponding serum calcium levels. Using calcium and citrate clamp techniques, we found that the response of the parathyroid glands in acute and maintained hypercalcemia and hypocalcemia, and renal phosphate handling in patients with heavy proteinuria was not different from that of healthy subjects.
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PMID:Evaluation of the calcium-PTH axis and renal handling of phosphate by calcium and citrate clamp techniques in normal subjects and in patients with heavy proteinuria. 943 95

A family (a brother and a sister) of the familidal isolated hyperparathyroidism (FIH) was reported. The older brother with age of 58 year-old was pointed out hypercalcemic while examining his hypertension and proteinuria. He had high levels of serum total and ionized calcium, intact-PTH and gastrin, and hypophosphatemia. His neck CT scan revealed swelling of the two parathyroid glands in each side. He underwent resection of the tumors and the auto-implantation of the glands under diagnosis of primary hyper parathyroidism. Histopathology was diagnosed to be hyperplasia of the parathyroid glands. The younger sister with age of 52 year-old was referred to our clinic because she was suffering from recurrent urolithiasis. Biochemical examination of her blood sampling resulted in very resemble values of her brother mentioned above. Her neck CT scan showed three tumors consisting of each one at the bilateral parathyroid glands and one in the thymic region. She underwent resection of the tumors and the auto-implantation of the glands and histopathological diagnosis was hyperplasia as same as her brother's one. The postoperative courses of these cases have been uneventful for four years. FIH is a low significant disease of which ten lineages have been reported in Japanese literature although it should be differentiate with such a disease of multiple endocrine neoplasms.
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PMID:[Familial isolated hyperparathyroidism: a report of two cases]. 1068 81

Here we report on a patient with findings of acrocephaly, craniosynostosis, low frontal hairline, ptosis of eyelids, deviated nasal septum, broad great toes, moderate hallux valgus, bilateral symmetrical complete soft tissue syndactyly of toes 2 and 3, and partial soft tissue syndactyly of toes 4 and 5 consistent with the diagnosis of Saethre-Chotzen syndrome. Additionally, the patient had some unusual findings as part of generalized dysfunction of the renal tubules including hypophosphatemia with renal phosphate wasting, normocalcemic hypercalciuria, hypomagnesemia with renal magnesium wasting, low-molecular-weight proteinuria, decreased serum PTH levels, osteopenia, and nephrolithiasis. In the light of these findings, the diagnosis of incomplete renal Fanconi syndrome was made. In conclusion, on the basis of the present findings, it is difficult to say whether renal tubular dysfunction are somehow connected to the Saethre-Chotzen syndrome or not. Therefore, we consider that this is probably just a coincident. However, further studies may show the connection between renal tubular dysfunction and Saethre-Chotzen syndrome.
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PMID:Saethre-Chotzen syndrome presenting with incomplete renal Fanconi syndrome. 1221 32

Conservative treatment implies procedures which involve normalization or improvement of metabolic disorders in chronic renal insufficiency and failure by medicamentous and dietary means. Keto amino acids administration can remarkable influence protein synthesis, metabolic acidosis, Ca-P and PTH levels, carbohydrate and lipid disorders, but has no effect on hyperfiltration. Long-term co-administration of rHuEPO and keto amino acids in CRF patients on LPD has accelerated metabolic effect associated with a delay in progression of renal failure and reduction of proteinuria. Also, concomitant administration of ACE inhibitors and angiotensin II AT1 receptor antagonist in CRF patients on LPD with KA was associated with significant decrease of proteinuria, amino-aciduria and, via its glomerulo-tubular action, it had also an effect on progression of CRF.
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PMID:[Present opinions on use of ketoanalog essential aminoacids in a conservative treatment of chronic renal insufficiency]. 1532 64


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