Nephrotic syndrome

2020 ◽  
Vol 13 (3) ◽  
pp. 159-163
Author(s):  
Thuvaraka Ware

Nephrotic syndrome is characterised by proteinuria, hypoalbuminaemia and oedema. The renal function is often normal and symptoms may mimic other common pathologies presenting in the community. The underlying aetiology is more heterogenous in adults compared with children, further confounding the diagnostic process and leading to delays in recognition. It is a relatively rare presentation in primary care, but the consequences of nephrotic syndrome can be significant. Complications include hyperlipidaemia, hypercoaguability, increased risk of infection and end-stage renal failure. It is, therefore, important to diagnose, investigate and manage nephrotic syndrome appropriately.

2017 ◽  
Vol 68 (6) ◽  
pp. 1325-1328
Author(s):  
Andrada Raluca Doscas ◽  
Mihail Balan ◽  
Mihai Liviu Ciofu ◽  
Doriana Agop Forna ◽  
Marius Cristian Martu ◽  
...  

Chronic kidney disease (CKD) is a multifactorial syndrome and a global health concern. As renal function declines, there is a progressive deterioration of mineral homeostasis. Starting from stage 3 of CKD oral manifestations of mineral disorders can occasionally appear and become more frequent and evident in stage 5. We retrospectively analysed 43 patients diagnosed with end stage renal failure undergoing dialysis, hospitalized in our clinic for different oral and maxillofacial pathologies. The mean dialysis period was 5.43 years. Radiographic alterations afecting the jaws were found in all patients. The most common feature was partial or total loss of lamina dura, followed by alterations of the bony trabeculae. 9 patients presented brown tumors which are considered the final stage of secondary hyperparathyroidism associated with renal failure.


1987 ◽  
Vol 20 (2) ◽  
pp. 105-109
Author(s):  
Kazumasa Shimamatsu ◽  
Satoru Fujimi ◽  
Kaoru Onoyama ◽  
Hiroshi Tsuruda ◽  
Masatoshi Fujishima

2002 ◽  
Vol 13 (2) ◽  
pp. 400-405 ◽  
Author(s):  
Yaacov Frishberg ◽  
Choni Rinat ◽  
Orli Megged ◽  
Eli Shapira ◽  
Sofia Feinstein ◽  
...  

ABSTRACT. Steroid-resistant nephrotic syndrome (SRNS) represents a heterogeneous group of kidney disorders that are often resistant to other immunosuppressive agents and tend to progress to end-stage renal failure. Mutations in the gene NPHS2 that encode a protein named podocin have recently been found in a recessive form of SRNS. Ten children from two inbred families of Israeli-Arab descent presented with SRNS. Renal histologic findings were of diffuse mesangial proliferation. Six patients reached end-stage renal failure, but nephrotic syndrome did not recur after renal transplantation. Mutation analysis of NPHS2 revealed that they were homozygous for the C412T mutation (R138X). Eighteen children were subsequently analyzed with SRNS due to biopsy-proven focal segmental glomerulosclerosis (FSGS) from unrelated families of Israeli-Arab descent. Analysis disclosed six additional patients (33%) bearing the same mutation in a homozygous pattern. Three of them had no affected relatives, although they came from large families. Taken together, of the 27 patients tested (familial and nonfamilial), 15 patients (55%) were homozygous for the mutation (R138X). They all shared the same haplotype and were homozygous for the A1023G polymorphism, thus pointing to a possible founder effect. Thirteen children of Israeli-Jewish origin with SRNS and biopsy-proven FSGS and 15 children of both ethnic groups with steroid-responsive FSGS were tested, and none was found to have mutations in NPHS2. The results of this study demonstrate that mutations in NPHS2 are a common cause of SRNS in Israeli-Arab children. Mutations in NPHS2 may cause SRNS in nonfamilial cases. The interethnic differences in the occurrence of NPHS2 mutations may explain, in part, the previous observation that Arab patients with FSGS in Israel have a worse prognosis as compared with Jewish patients, despite similar presenting symptoms and medical management. Identifying the causing mutation will enable clinicians to avoid unnecessary immunosuppressive therapeutic trials in newly diagnosed patients and to provide prenatal diagnosis to families at risk.


1997 ◽  
Vol 77 (04) ◽  
pp. 650-655 ◽  
Author(s):  
R Vanholder ◽  
A Camez ◽  
N Veys ◽  
A Van Loo ◽  
A M Dhondt ◽  
...  

SummaryRecently, hirudin was used for the first time as an anticoagulant during hemodialysis in men. Pharmacokinetic data of this compound in end-stage renal failure are however not available. In this study, the pharmacokinetics of recombinant hirudin (HBW 023) was evaluated in hemodialysis-treated end-stage renal failure patients. HBW 023 was administered as a bolus at the start of a single dialysis (0.02 to 0.08 mg/kg) in 20 patients, and plasma hirudin levels were followed during this and the 5 following dialyses, without additional hirudin administration. The initial dialysis (HDj) was performed with a low flux polysulfone dialyzer; the following dialyses (up to HD6) with a high flux polysulfone dialyzer and regular heparin. Hirudin levels averaged 504.0 ± 214.0 and 527.7 ± 217.1 ng/ml in the middle and at the end of HDj, and then gradually decreased to 15.2 ± 15.2 ng/ml at the end of HD6. Pharmacokinetic data were compared to those obtained in healthy controls (n = 5), receiving the same dose, and reaching the same peak hirudin level. Hirudin half-life was >30 times longer in hemodialysis patients (51.8 ± 15.6 vs. 1.7 ± 1.5 h, p <0.001), whereas area under the curve was >60 times higher (34,669 ± 14,898 vs. 545 ± 205 ng/ml X h, p <0.001). Distribution volume was lower in hemodialysis patients (11.0 ± 3.1 vs. 14.1 ± 2.0 1, p <0.05). Hirudin disappearance rate was the same during high flux polysulfone dialysis as during interdialytic periods. Hirudin removal was markedly higher in those patients still maintaining some residual renal function and parameters of hirudin removal were significantly correlated to residual creatinine clearance. It is concluded that hirudin removal from the body is markedly depressed in hemodialyzed end-stage renal failure patients and that even minor residual renal function may increase this removal rate.


1989 ◽  
Vol 12 (11) ◽  
pp. 688-691 ◽  
Author(s):  
R.J. Caruana

First-use reactions comprise a spectrum of adverse clinical signs and symptoms occurring in end-stage renal failure patients during hemodialysis treatments. This report describes four patients experiencing first-use reactions in the context of being referred to or from a tertiary care inpatient dialysis facility. Theories on the pathogenesis of first-use reactions are reviewed and recommendations for identifying patients at increased risk for this problem are proposed.


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