scholarly journals Successful Management of Repetitive Urinary Obstruction and Anuria Caused by Double J Stent Calculi Formation after Renal Transplantation

2014 ◽  
Vol 2014 ◽  
pp. 1-3
Author(s):  
Zongyao Hao ◽  
Li Zhang ◽  
Jun Zhou ◽  
Xiansheng Zhang ◽  
Haoqiang Shi ◽  
...  
Keyword(s):  
Renal Transplantation ◽  
Clinical Manifestations ◽  
Lower Abdominal Pain ◽  
Good Recovery ◽  
Successful Management ◽  
Dihydroxyvitamin D3 ◽  
Double J Stent ◽  
Renal Tubular Reabsorption ◽  
Renal Tubular

This report firstly describes an extremely rare case of repetitive double J stent calculi formation after renal transplantation caused by the antihyperparathyroidism (HPT) drug calcitriol. In 2012, a woman initially presented to our hospital for anuria with lower abdominal pain. She was diagnosed with allograft hydronephrosis and double J stents obstruction by calculi formation after transplantation and treated with triplicate stents replacements in another hospital without clinical manifestations improvements. Through detailed exploration of medical history, we conclude that the abnormal calculi formation is due to the calcitriol (1,25-dihydroxyvitamin D3) administration, a drug which can increase renal tubular reabsorption of calcium for treating posttransplant HPT bone disease. After discontinuing calcitriol, the patient was stone-free and had a good recovery without severe complications during the 9-month follow-up. Our novel findings may provide an important clue and approach to managing formidable repetitive double J stent calculi formation in the clinical trial.

scholarly journals Early post-transplantation hypophosphatemia is associated with elevated FGF-23 levels

2011 ◽  
Vol 164 (5) ◽  
pp. 839-847 ◽  
Author(s):  
Andrea Trombetti ◽  
Laura Richert ◽  
Karine Hadaya ◽  
Jean-Daniel Graf ◽  
François R Herrmann ◽  
...  
Keyword(s):  
Renal Transplantation ◽  
Tubular Reabsorption ◽  
Phosphate Metabolism ◽  
Multivariate Models ◽  
Intact Pth ◽  
Post Transplantation ◽  
Estimated Gfr ◽  
Renal Tubular Reabsorption ◽  
Renal Tubular ◽  
Fgf 23

BackgroundWe examined the hypothesis that high FGF-23 levels early after transplantation contribute to the onset of hypophosphatemia, independently of parathyroid hormone (PTH) and other factors regulating phosphate metabolism.MethodsWe measured serum phosphate levels (sPi), renal tubular reabsorption of Pi (TmPi/GFR), estimated GFR (eGFR), intact PTH (iPTH), calcitriol, intact (int) and C-terminal (Cter) FGF-23, dietary Pi intake and cumulative doses of glucocorticoids in 69 patients 12 days (95% confidence interval, 10–13) after renal transplantation.ResultsHypophosphatemia was observed in 43 (62%) of the patients 12 days after transplantation. Compared with non-hypophosphatemic subjects, their post-transplantation levels of intact and CterFGF-23 were higher (195 (108–288) vs 48 (40–64) ng/l, P<0.002 for intFGF-23; 205 (116–384) vs 81 (55–124) U/ml, P<0.002, for CterFGF-23). In all subjects, Cter and intFGF-23 correlated inversely with sPi (r=−0.35, P<0.003; −0.35, P<0.003, respectively), and TmPi/GFR (r=−0.50, P<0.001; −0.54, P<0.001, respectively). In multivariate models, sPi and TmPi/GFR were independently associated with FGF-23, iPTH and eGFR. Pre-transplant iPTH levels were significantly higher in patients developing hypophosphatemia after renal transplantation. Pre-transplant levels of FGF-23 were not associated with sPi at the time of transplantation.ConclusionIn addition to PTH, elevated FGF-23 may contribute to hypophosphatemia during the early post-renal transplant period.

Contrasting effects of intravenous and oral etidronate on vitamin D metabolism in man

1988 ◽  
Vol 74 (1) ◽  
pp. 101-106 ◽  
Author(s):  
P. J. Lawson-Matthew ◽  
D. F. Guilland-Cumming ◽  
A. J. P. Yates ◽  
R. G. G. Russell ◽  
J. A. Kanis
Keyword(s):  
Vitamin D ◽  
Urinary Excretion ◽  
Progressive Increase ◽  
Urinary Calcium ◽  
Calcium Excretion ◽  
Vitamin D Metabolism ◽  
Dihydroxyvitamin D3 ◽  
Renal Tubular Reabsorption ◽  
Early Effects ◽  
Renal Tubular

1. We have studied the early effects of intravenously and orally administered etidronate on vitamin D metabolism and indirect indices of calcium and skeletal metabolism in 17 patients with Paget's disease of bone. 2. Administration of etidronate by mouth (700–1400 mg daily for 1 month) or its intravenous infusion (300 mg daily for 5 days) decreased bone resorption as judged by urinary excretion of hydroxyproline and significantly increased renal tubular reabsorption of phosphate. No significant change in serum activity of alkaline phosphatase was noted with either regimen. 3. When etidronate was given by mouth there was a progressive decrease in fasting urinary calcium excretion and a rise in serum 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3]. In contrast, intravenous etidronate decreased serum values of l,25-(OH)2D3 and was associated with a progressive increase in fasting calcium excretion, suggesting a decrease in the net influx of calcium from the extracellular compartment to bone. Significant inverse correlations were noted between the change induced in 1,25-(OH)2D3 values at 2 weeks and the changes in serum calcium, phosphate and fasting urinary excretion of calcium. 4. These observations suggest that the different effects of intravenous and oral etidronate on l,25-(OH)2D3 values are a consequence of different doses of etidronate used and the different effects of these regimens on the accretion of calcium into bone.

Clinical Analysis of Primary Primitive Neuroectodermal Tumors in the Female Genital Tract

2014 ◽  
Vol 24 (3) ◽  
pp. 404-409 ◽  
Author(s):  
Changji Xiao ◽  
Jing Zhao ◽  
Peng Guo ◽  
Dan Wang ◽  
Dachun Zhao ◽  
...  
Keyword(s):  
Genital Tract ◽  
Female Genital Tract ◽  
Clinical Manifestations ◽  
Neuron Specific Enolase ◽  
Lower Abdominal Pain ◽  
Primitive Neuroectodermal Tumors ◽  
Pathologic Features ◽  
Neuroectodermal Tumors ◽  
Female Genital

ObjectiveThe aim of the study was to investigate the clinical manifestations, diagnosis, treatment, and prognosis of primitive neuroectodermal tumors (PNETs) in the female genital tract.MethodsFrom April 2001 to May 2013, the clinicopathologic characteristics, treatments, outcomes, and prognosis of 11 patients with PNET in the female genital tract were analyzed retrospectively at our hospital.ResultsThe location of PNET in the 11 patients presented here included vulva (2 patients), cervix (2 patients), uterus and its ligament (5 patients), and the ovaries (2 patients). Ages ranged from 18 to 59 years (median, 31 years).The main clinical manifestations of PNET in the female genital tract are irregular vaginal bleeding (6 patients), pelvic mass, uterine enlargement, and rapidly increasing vulvar mass (8 patients), and vulvar pain and lower abdominal pain (5 patients). The CA125 levels of 8 patients were elevated before the operations and reduced to normal when the diseases were controlled, while the levels increased as the tumor was progressive. Results for the most commonly used immunohistochemistry studies revealed CD99 in 11 of the 11 tumors, synaptophysin in 6 of the 7 positive tumors, and neuron-specific enolase in 6 of the 6 tumors. Ten patients underwent surgical resection. Nine of them underwent preoperative or/and postoperative combination chemotherapy. The follow-up of 10 patients were available and ranged from 1 to 145 months (median, 30.5 months), 3 of whom experiencing recurrence.ConclusionsPrimitive neuroectodermal tumor is very rare and can originate from any part of the female genital tract. The tumors had different manifestations but the same pathologic features. CA125 may be an important marker for prognosis and follow-up of PNET of the female internal genital tract.

Hypercalcemia in children

2020 ◽  
Vol 24 (2) ◽  
pp. 42-51
Author(s):  
S. V. Papizh
Keyword(s):  
Calcium Homeostasis ◽  
Clinical Manifestations ◽  
Trigger Factors ◽  
Physiological Mechanisms ◽  
Blood Calcium ◽  
Severe Hypercalcemia ◽  
Wide Range ◽  
Renal Tubular Reabsorption ◽  
Renal Tubular ◽  
Neonates And Infants

Hypercalcemia is a result of a wide range of hereditary and acquired conditions encountered by general physicians and pediatricians. Calcium participates in several key physiological functions, control of blood coagulation, bone calcification. Calcium homeostasis is tightly regulated by the interplay between absorption from the small intestine and renal tubular reabsorption, bone remodeling, and disposal through the gut and the kidney. These processes are regulated by local and circulating factors. The two main hormones influencing the homeostasis of calcium are PTH and calcitriol. Cancer-associated hypercalcemia and primary hyperparathyroidism are the most frequent causes of hypercalcemia in adults. In neonates and infants, one should look first at genetic and iatrogenic etiologies. The clinical manifestations of hypercalcemia in children are nonspecific due to damage to various organs and systems and depend on the degree of blood calcium level. Mild hypercalcemia is asymptomatic and often discovered during routine blood work. Moderate and severe hypercalcemia may cause cardiac arrhythmias, affect the nervous system. The differential diagnosis of the possible etiologies of hypercalcemia should start with the assessment of serum parathyroid hormone (PTH) concentration. The causes of hypercalcemia can be divided between PTH-mediated and non-PTH-mediated. Identification of the main causes of hypercalcemia contributes to the timely elimination of trigger factors, beginning of treatment, correction of nutrition and lifestyle. The article highlights physiological mechanisms of calcium homeostasis, clinical manifestations, diagnostic algorithms and treatment of hypercalcemia in children.

IMMUNOREACTIVE GROWTH HORMONE IN PLASMA AND URINE IN JUVENILE DIABETICS BEFORE AND DURING INITIAL INSULIN TREATMENT

1974 ◽  
Vol 75 (1) ◽  
pp. 50-63 ◽  
Author(s):  
Kristian F. Hanssen
Keyword(s):  
Growth Hormone ◽  
Insulin Treatment ◽  
Juvenile Diabetes ◽  
Control Group ◽  
List Type ◽  
Newly Diagnosed ◽  
Renal Tubular Reabsorption ◽  
Juvenile Diabetics ◽  
The Mean ◽  
Renal Tubular

ABSTRACT Twenty newly diagnosed, but as yet untreated patients of both sexes with classical juvenile diabetes were investigated by determining the mean plasma immunoreactive growth hormone (IRHGH) and urinary IRHGH for a 24 hour period before and during initial insulin treatment. The plasma IRHGH was significantly higher (0.05 > P > 0.01) before than during initial insulin treatment. During initial insulin treatment, the mean plasma IRHGH was significantly higher (0.01 > P > 0.001) than in a control group. The urinary IRHGH was significantly higher (0.01 > P > 0.001) before than during insulin treatment. The increased urinary IRHGH observed before insulin treatment is thought to be partly due to a defective renal tubular reabsorption of growth hormone. No significant correlation was found between the mean blood sugar and plasma or urinary IRHGH either before or during insulin treatment.

Monogenic Diabetes: Genetics and Relevance on Diabetes Mellitus Personalized Medicine

2020 ◽  
Vol 16 (8) ◽  
pp. 807-819 ◽  
Author(s):  
Madalena Sousa ◽  
Jácome Bruges-Armas
Keyword(s):  
Diabetes Mellitus ◽  
Complex Disease ◽  
Clinical Manifestations ◽  
Neonatal Diabetes ◽  
Monogenic Diabetes ◽  
Diabetes Genetics ◽  
Individualize Treatment

Background: Diabetes mellitus (DM) is a complex disease with significant impression in today's world. Aside from the most common types recognized over the years, such as type 1 diabetes (T1DM) and type 2 diabetes (T2DM), recent studies have emphasized the crucial role of genetics in DM, allowing the distinction of monogenic diabetes. Methods: Authors did a literature search with the purpose of highlighting and clarifying the subtypes of monogenic diabetes, as well as the accredited genetic entities responsible for such phenotypes. Results: The following subtypes were included in this literature review: maturity-onset diabetes of the young (MODY), neonatal diabetes mellitus (NDM) and maternally inherited diabetes and deafness (MIDD). So far, 14 subtypes of MODY have been identified, while three subtypes have been identified in NDM - transient, permanent, and syndromic. Discussion: Despite being estimated to affect approximately 2% of all the T2DM patients in Europe, the exact prevalence of MODY is still unknown, accentuating the need for research focused on biomarkers. Consequently, due to its impact in the course of treatment, follow-up of associated complications, and genetic implications for siblings and offspring of affected individuals, it is imperative to diagnose the monogenic forms of DM accurately. Conclusion: Currently, advances in the genetics field allowed the recognition of new DM subtypes, which until now, were considered slight variations of the typical forms. Thus, it is imperative to act in the close interaction between genetics and clinical manifestations, to facilitate diagnosis and individualize treatment.

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