Pub Date : 2020-05-27DOI: 10.24966/nrt-7313/100027
Mohammad Abuzeineh
Renal transplant, when possible, is the treatment of choice for patients with advanced renal failure approaching End Stage Renal Disease (ESRD). Unfortunately, there is a significant gap between supply and demand for available kidney transplants. With the 2014 updated Kidney Allocation System (KAS), patients with older age have shorter expected post-transplant survival, thus have less chances to get transplanted. In this case report, we describe a 76 year-old male who underwent a successful deceased renal transplant from a donor who had known Autosomal Dominant Polycystic Kidney Disease (ADPKD). His chances of having an “ordinary” kidney were low; hence we opted to offer him a rather “unordinary” kidney, which was successfully transplanted with near normal post-transplant renal allograft function. This case report presents a silver lining for aging ESRD population, with a chance to improve their survival and quality of life by keeping them off dialysis.
{"title":"Transplanting A Polycystic Kidney; Trojan Horse Or Silver Lining","authors":"Mohammad Abuzeineh","doi":"10.24966/nrt-7313/100027","DOIUrl":"https://doi.org/10.24966/nrt-7313/100027","url":null,"abstract":"Renal transplant, when possible, is the treatment of choice for patients with advanced renal failure approaching End Stage Renal Disease (ESRD). Unfortunately, there is a significant gap between supply and demand for available kidney transplants. With the 2014 updated Kidney Allocation System (KAS), patients with older age have shorter expected post-transplant survival, thus have less chances to get transplanted. In this case report, we describe a 76 year-old male who underwent a successful deceased renal transplant from a donor who had known Autosomal Dominant Polycystic Kidney Disease (ADPKD). His chances of having an “ordinary” kidney were low; hence we opted to offer him a rather “unordinary” kidney, which was successfully transplanted with near normal post-transplant renal allograft function. This case report presents a silver lining for aging ESRD population, with a chance to improve their survival and quality of life by keeping them off dialysis.","PeriodicalId":92035,"journal":{"name":"HSOA journal of nephrology & renal therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46044337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-07-18DOI: 10.24966/nrt-7313/100021
R. Gordillo de Anda
The errors in the Mitochondrial DNA affects tissues that require highly dependent of energy to work properly like the Brain, the Heart, the Muscle and the Kidneys, the defects in the genesis of ATP affects this tissues sometimes involving more than one organ, therefore myophaties, encephalophaties, can be associated with renal diseaseswich rare in adults and more frequently in children in whom arefrequently unsuspected and underestimated. Their prevavalence in the general population is also underestimated and may be as high as 1-2:10,000 live births.
{"title":"Mitochondrial DNA Mutations and its Role in the Genesis of Renal Diseases an Update","authors":"R. Gordillo de Anda","doi":"10.24966/nrt-7313/100021","DOIUrl":"https://doi.org/10.24966/nrt-7313/100021","url":null,"abstract":"The errors in the Mitochondrial DNA affects tissues that require highly dependent of energy to work properly like the Brain, the Heart, the Muscle and the Kidneys, the defects in the genesis of ATP affects this tissues sometimes involving more than one organ, therefore myophaties, encephalophaties, can be associated with renal diseaseswich rare in adults and more frequently in children in whom arefrequently unsuspected and underestimated. Their prevavalence in the general population is also underestimated and may be as high as 1-2:10,000 live births.","PeriodicalId":92035,"journal":{"name":"HSOA journal of nephrology & renal therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47018634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-07-18DOI: 10.24966/NRT-7313/100020
R. Nashawati
Minimal Change Disease (MCD) represents the most common type of nephrotic syndrome in children (~80%), whereas in adults it accounts for 10% to 20% of cases. It seems to be associated with pollen allergy, asthma, NSAIDS use, and Hypoxia. A 25 years old girl with edema in both legs and facial puffiness and no other complain came to the clinic, her lab test was normal except for proteinuria 3.34g/24h and blood Albumin 1.9mg/dl, her ultrasonography for the kidneys was normal. Kidney Biopsy was normal and IF study was negative for immune related diseases. She was treated with corticosteroid; cyclosporine then tacrolimus so she could have good response.
{"title":"Minimal Change Disease in Young Adults: A Case Report","authors":"R. Nashawati","doi":"10.24966/NRT-7313/100020","DOIUrl":"https://doi.org/10.24966/NRT-7313/100020","url":null,"abstract":"Minimal Change Disease (MCD) represents the most common type of nephrotic syndrome in children (~80%), whereas in adults it accounts for 10% to 20% of cases. It seems to be associated with pollen allergy, asthma, NSAIDS use, and Hypoxia. A 25 years old girl with edema in both legs and facial puffiness and no other complain came to the clinic, her lab test was normal except for proteinuria 3.34g/24h and blood Albumin 1.9mg/dl, her ultrasonography for the kidneys was normal. Kidney Biopsy was normal and IF study was negative for immune related diseases. She was treated with corticosteroid; cyclosporine then tacrolimus so she could have good response.","PeriodicalId":92035,"journal":{"name":"HSOA journal of nephrology & renal therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42245022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-07-18DOI: 10.24966/NRT-7313/100022
L. RizoTopete
{"title":"Case Report of an Atypical Evolution of Urine Obstruction, is this Acute on Chronic Kidney Disease?","authors":"L. RizoTopete","doi":"10.24966/NRT-7313/100022","DOIUrl":"https://doi.org/10.24966/NRT-7313/100022","url":null,"abstract":"","PeriodicalId":92035,"journal":{"name":"HSOA journal of nephrology & renal therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45046277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-07-18DOI: 10.24966/NRT-7313/100023
R. Madhyastha
{"title":"An Unusual Case of Acute Kidney Injury with Edematous Kidneys and Venous Micro Thrombi: A Case Report","authors":"R. Madhyastha","doi":"10.24966/NRT-7313/100023","DOIUrl":"https://doi.org/10.24966/NRT-7313/100023","url":null,"abstract":"","PeriodicalId":92035,"journal":{"name":"HSOA journal of nephrology & renal therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46751195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-11-21DOI: 10.24966/nrt-7313/100016
A. Mahmood
Citation: Mahmood A Mineral Bone Disorder in Chronic Kidney Dis- ease, Mechanics and Management. J Nephrol Renal Ther 4: 016. rise in plasma phosphate resulting into hypocalcaemia and inhibition of calcitriol [9-11]. These changes result into secondary hyperparathyroidism [12-14] which contribute further to phosphate load due to mobilization of phosphate and calcium from the bone as a corrective attempt. Additionally proximal tubular phosphate reab-sorption continues to rise due to its reduced excretion with progression of renal failure. Initial rise of PTH is beneficial in order to maintain phosphate balance, correction of hypocalcaemia and calcitriol but hyperphosphatemia over prolong period results into autonomous parathyroid gland with rising secretions as a consequence of skeletal resistance with advanced renal failure [11]. Hyperphosphatemia has direct stimulatory effect on PTH independent of calcium and calcitriol levels [15-18]. Another effect of hyperparathyroidism is high fibroblast growth factor 23 (FGF 23), decrease vitamin D, Calcium Sensing Receptors (CaSR), fibroblast receptors and klotho in PTH. FGF 23 is the main factor causing low calcitriol, not reduce neph-ron mass [10] as a result of inhibition of enzyme 1 alpha hydroxy-lase which converts 25 hydroxy vitamin D to calcitriol. FGF 23 is produced from osteocytes in response to high phosphate, calcitriol and renal injury and establish its phosphaturic effect with the help of coenzyme klotho [19] to maintain phosphate homeostasis. It`s clearance is decrease in CKD. Reduced calcitriol levels stimulate PTH [20-22] by mechanism which decrease absorption from the gut and reduce mobilization from the bones resulting into hypocalcemic state triggering PTH activation resulting in release of hormone. Abstract Bone health is seriously affected in Chronic Kidney Disease (CKD). Subtle changes begin from the initial stages. Skeletal ill ef- fects are related to imbalance homeostasis of four main players, calcium, phosphate, Parathyroid Hormone (PTH) and vitamin D. Their regulated action is important and interdependent for normal skeletal development, architectural integrity and strength. Dysregu- lation in these regulators result in progressive skeletal dystrophy if mechanism goes unnoticed which imparts extra skeletal deleterious effects with grave long term consequences in terms of bone pain, fractures, vascular, valvular and soft tissue calcification. Term renal osteodystrophy has been replaced by Mineral Bone Disorder (MBD) which include spectrum of diseases like adynamic bone disease, osteomalacia, osteitis fibrosa cystica, osteopenia and osteoporo -sis. Close surveillance with CKD stage appropriate investigations and timely action is crucial to detect and prevent skeletal and extra skeletal complications in order to minimize morbidity and mortality in CKD population with the outcome of improved quality adjusted life years. This article will help improve our understanding about the highl
{"title":"Mineral Bone Disorder in Chronic Kidney Disease, Mechanics and Management","authors":"A. Mahmood","doi":"10.24966/nrt-7313/100016","DOIUrl":"https://doi.org/10.24966/nrt-7313/100016","url":null,"abstract":"Citation: Mahmood A Mineral Bone Disorder in Chronic Kidney Dis- ease, Mechanics and Management. J Nephrol Renal Ther 4: 016. rise in plasma phosphate resulting into hypocalcaemia and inhibition of calcitriol [9-11]. These changes result into secondary hyperparathyroidism [12-14] which contribute further to phosphate load due to mobilization of phosphate and calcium from the bone as a corrective attempt. Additionally proximal tubular phosphate reab-sorption continues to rise due to its reduced excretion with progression of renal failure. Initial rise of PTH is beneficial in order to maintain phosphate balance, correction of hypocalcaemia and calcitriol but hyperphosphatemia over prolong period results into autonomous parathyroid gland with rising secretions as a consequence of skeletal resistance with advanced renal failure [11]. Hyperphosphatemia has direct stimulatory effect on PTH independent of calcium and calcitriol levels [15-18]. Another effect of hyperparathyroidism is high fibroblast growth factor 23 (FGF 23), decrease vitamin D, Calcium Sensing Receptors (CaSR), fibroblast receptors and klotho in PTH. FGF 23 is the main factor causing low calcitriol, not reduce neph-ron mass [10] as a result of inhibition of enzyme 1 alpha hydroxy-lase which converts 25 hydroxy vitamin D to calcitriol. FGF 23 is produced from osteocytes in response to high phosphate, calcitriol and renal injury and establish its phosphaturic effect with the help of coenzyme klotho [19] to maintain phosphate homeostasis. It`s clearance is decrease in CKD. Reduced calcitriol levels stimulate PTH [20-22] by mechanism which decrease absorption from the gut and reduce mobilization from the bones resulting into hypocalcemic state triggering PTH activation resulting in release of hormone. Abstract Bone health is seriously affected in Chronic Kidney Disease (CKD). Subtle changes begin from the initial stages. Skeletal ill ef- fects are related to imbalance homeostasis of four main players, calcium, phosphate, Parathyroid Hormone (PTH) and vitamin D. Their regulated action is important and interdependent for normal skeletal development, architectural integrity and strength. Dysregu- lation in these regulators result in progressive skeletal dystrophy if mechanism goes unnoticed which imparts extra skeletal deleterious effects with grave long term consequences in terms of bone pain, fractures, vascular, valvular and soft tissue calcification. Term renal osteodystrophy has been replaced by Mineral Bone Disorder (MBD) which include spectrum of diseases like adynamic bone disease, osteomalacia, osteitis fibrosa cystica, osteopenia and osteoporo -sis. Close surveillance with CKD stage appropriate investigations and timely action is crucial to detect and prevent skeletal and extra skeletal complications in order to minimize morbidity and mortality in CKD population with the outcome of improved quality adjusted life years. This article will help improve our understanding about the highl","PeriodicalId":92035,"journal":{"name":"HSOA journal of nephrology & renal therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46449654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-11-21DOI: 10.24966/NRT-7313/100017
R. Gaeta
X-linked Alport syndrome is a rare hereditary disorder caused by variants of the COL4A5 gene. We describe a case of a 28 year old Caucasian male with a family history of end-stage renal disease presenting with episodic gross hematuria and nephrotic range proteinuria. Renal biopsy demonstrated focal segmental glomerulosclerosis with non-diagnostic ultrastructural findings. Next Generation Sequencing revealed a COL4A5 missense likely pathogenic variant, a substitution of adenine for guanine at nucleotide 901(c.901G>A) of the coding DNA predicting a glycine to serine substitution at amino acid 301 (p.Glyc301Ser). This variant has not been reported in literature or human genomic databases.
{"title":"A Case Report of a Novel Variant of X-linked Alport Syndrome","authors":"R. Gaeta","doi":"10.24966/NRT-7313/100017","DOIUrl":"https://doi.org/10.24966/NRT-7313/100017","url":null,"abstract":"X-linked Alport syndrome is a rare hereditary disorder caused by variants of the COL4A5 gene. We describe a case of a 28 year old Caucasian male with a family history of end-stage renal disease presenting with episodic gross hematuria and nephrotic range proteinuria. Renal biopsy demonstrated focal segmental glomerulosclerosis with non-diagnostic ultrastructural findings. Next Generation Sequencing revealed a COL4A5 missense likely pathogenic variant, a substitution of adenine for guanine at nucleotide 901(c.901G>A) of the coding DNA predicting a glycine to serine substitution at amino acid 301 (p.Glyc301Ser). This variant has not been reported in literature or human genomic databases.","PeriodicalId":92035,"journal":{"name":"HSOA journal of nephrology & renal therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41950696","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-11-21DOI: 10.24966/NRT-7313/100019
Iyad Abuward Abu-sharkh
Schmidt Syndrome refers to the combination of autoimmune adrenal insufficiency (Addison’s disease) with autoinmune thyroiditis, and is part of a larger syndrome known as autoinmune polyendocrine syndrome type II or polyglandular autoinmune syndrome type II (PAS II). Schmidt Syndrome as a 1:20,000 prevalence in general population with 3:1 ratio of females to males affected. It is autosomal dominant inheritance with variable penetrance. Associated with certain HLA antigens HLA-DR3, HLA-DR4, non HLA gene M-ICA and CTLA-4. The diagnosis of the Schmidt Syndrome is the same as that of the individual disorders. The treatment includes of primary hypothyroidism and the Addison disease. We present the evolution, the clinic and the treatment of a patient diagnosed with Schmidt Syndrome.
{"title":"Debut of Polyglandular Autoimmune Syndrome Type 2 (Schmidt Syndrome) in a Patient with Chronic Kidney Disease of Unknown Etiology in Peritoneal Dialysis","authors":"Iyad Abuward Abu-sharkh","doi":"10.24966/NRT-7313/100019","DOIUrl":"https://doi.org/10.24966/NRT-7313/100019","url":null,"abstract":"Schmidt Syndrome refers to the combination of autoimmune adrenal insufficiency (Addison’s disease) with autoinmune thyroiditis, and is part of a larger syndrome known as autoinmune polyendocrine syndrome type II or polyglandular autoinmune syndrome type II (PAS II). Schmidt Syndrome as a 1:20,000 prevalence in general population with 3:1 ratio of females to males affected. It is autosomal dominant inheritance with variable penetrance. Associated with certain HLA antigens HLA-DR3, HLA-DR4, non HLA gene M-ICA and CTLA-4. The diagnosis of the Schmidt Syndrome is the same as that of the individual disorders. The treatment includes of primary hypothyroidism and the Addison disease. We present the evolution, the clinic and the treatment of a patient diagnosed with Schmidt Syndrome.","PeriodicalId":92035,"journal":{"name":"HSOA journal of nephrology & renal therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45436884","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-01-01Epub Date: 2016-03-10DOI: 10.24966/NRT-7313/100004
Ilse Daehn
{"title":"Shift in Focus-To Explore the Role of the Endothelium in Kidney Disease.","authors":"Ilse Daehn","doi":"10.24966/NRT-7313/100004","DOIUrl":"https://doi.org/10.24966/NRT-7313/100004","url":null,"abstract":"","PeriodicalId":92035,"journal":{"name":"HSOA journal of nephrology & renal therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5608090/pdf/nihms848347.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35440172","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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