scholarly journals Autosomal Dominant Polycystic Kidney Disease does not significantly alter major COVID-19 outcomes among veterans

2020 ◽  
Author(s):  
Xiangqin Cui ◽  
Julia W. Gallini ◽  
Christine L. Jasien ◽  
Michal Mrug
Keyword(s):  
Risk Factor ◽  
Kidney Disease ◽  
Kidney Diseases ◽  
Significant Risk ◽  
Significant Risk Factor ◽  
Cystic Kidney ◽  
Autosomal Dominant Polycystic Kidney ◽  
Cystic Liver ◽  
Cystic Kidney Diseases ◽  
Ventilator Requirement

AbstractChronic kidney disease (CKD), as well as its common causes (e.g., diabetes and obesity), are recognized risk factors for severe COVID-19 illness. To explore whether the most common inherited cause of CKD, autosomal dominant polycystic kidney disease (ADPKD), is also an independent risk factor, we studied data from the VA health system and the VA COVID-19-shared resources (e.g., ICD codes, demographics, pre-existing conditions, pre-testing symptoms, and post-testing outcomes). Among 61 COVID-19-positive ADPKD patients, 21 (34.4%) were hospitalized, 10 (16.4%) were admitted to ICU, 4 (6.6%) required ventilator, and 4 (6.6%) died by August 18, 2020. These rates were comparable to patients with other cystic kidney diseases and cystic liver-only diseases. ADPKD was not a significant risk factor for any of the four outcomes in multivariable logistic regression analyses when compared with other cystic kidney diseases and cystic liver-only diseases. In contrast, diabetes was a significant risk factor for hospitalization [OR 2.30 (1.61, 3.30), p<0.001], ICU admission [OR 2.23 (1.47, 3.42), p<0.001], and ventilator requirement [OR 2.20 (1.27, 3.88), p=0.005]. Black race significantly increased the risk for ventilator requirement [OR 2.00 (1.18, 3.44), p=0.011] and mortality [OR 1.60 (1.02, 2.51), p=0.040]. We also examined the outcome of starting dialysis after COVID-19 confirmation. The main risk factor for starting dialysis was CKD [OR 6.37 (2.43, 16.7)] and Black race [OR 3.47 (1.48, 8.1)]. After controlling for CKD, ADPKD did not significantly increase the risk for newly starting dialysis comparing with other cystic kidney diseases and cystic liver-only diseases. In summary, ADPKD did not significantly alter major COVID-19 outcomes among veterans when compared to other cystic kidney and liver patients.

scholarly journals Hypomagnesaemia is absent in children with autosomal dominant polycystic kidney disease

2018 ◽  
Vol 56 (1) ◽  
pp. 90-94 ◽  
Author(s):  
Tomáš Seeman ◽  
Magdaléna Fořtová ◽  
Bruno Sopko ◽  
Richard Průša ◽  
Michael Pohl ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Autosomal Dominant ◽  
Kidney Diseases ◽  
Differential Diagnostics ◽  
Cystic Kidney ◽  
Polycystic Kidney ◽  
Autosomal Dominant Polycystic Kidney ◽  
Cystic Kidney Diseases ◽  
Rule Out

Background Hypomagnesaemia is present in 40–50% of children with autosomal dominant renal cysts and diabetes syndrome (RCAD). On the contrary, the prevalence of hypomagnesaemia in children with autosomal dominant polycystic kidney disease (ADPKD) has never been examined. We aimed to investigate whether hypomagnesaemia is present in children with polycystic kidney diseases. Methods Children with cystic kidney diseases were investigated in a cross-sectional study. Serum concentrations of magnesium (S-Mg) and fractional excretion of magnesium (FE-Mg) were tested. Fifty-four children with ADPKD ( n = 26), autosomal recessive polycystic kidney disease (ARPKD) ( n = 16) and RCAD ( n = 12) with median age of 11.2 (0.6–18.6) years were investigated. Results Hypomagnesaemia (S-Mg < 0.7 mmol/L) was detected in none of the children with ADPKD/ARPKD and in eight children (67%) with RCAD. Median S-Mg in children with ADPKD/ARPKD was significantly higher than in children with RCAD (0.89 vs. 0.65 mmol/L, P < 0.01). The FE-Mg was increased in 23% of patients with ADPKD/ARPKD (all had chronic kidney disease stages 2–4) and in 63% of patients with RCAD, where it significantly correlated with estimated glomerular filtration rate (r = −0.87, P < 0.01). Conclusions Hypomagnesaemia is absent in children with ADPKD or ARPKD and could serve as a marker for differential diagnostics between ADPKD, ARPKD and RCAD in children with cystic kidney diseases of unknown origin where molecular genetic testing is lacking. However, while hypomagnesaemia, in the absence of diuretics, appears to rule out ADPKD and ARPKD, normomagnesaemia does not rule out RCAD at least in those aged <3 years.

MO026CLINICAL AND MUTATIONAL SPECTRUM OF CHILDREN WITH AUTOSOMAL RECESSIVE AND AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Ozum Tutal ◽  
Bora Gulhan ◽  
Emine Atayar ◽  
Selcuk Yuksel ◽  
Z Birsin Ozcakar ◽  
...  
Keyword(s):  
Renal Transplantation ◽  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Kidney Diseases ◽  
Cystic Kidney ◽  
Polycystic Kidney ◽  
Autosomal Dominant Polycystic Kidney ◽  
Cystic Kidney Diseases ◽  
Pkd2 Mutation

Abstract Background and Aims Cystic kidney diseases are a heterogeneous group of chronic renal disease. Autosomal recessive polycystic kidney disease (ARPKD) is generally diagnosed in utero or at birth due to mutations in PKHD1 gene. Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited kidney disease commonly associated with mutations in PKD1 or PKD2. In this study, we aimed to investigate clinical and genetic features of ARPKD and ADPKD in a group of Turkish patients. Method A total of 69 children with genetically confirmed ARPKD (10 females, 11 males) or ADPKD (28 females, 20 males) from seven pediatric nephrology centers were included in this study. Demographic features, family history, clinical and laboratory findings at presentation and during 12 months intervals were collected. Results For ARPKD patients, the median age at diagnosis was 10.5 (IQR; 0.75-58.5) months. Consanguinity between parents was present in 11 patients (52.4%). At the time of diagnosis, 14 (66.7%) patients had eGFR&lt;90 ml/min/1.73 m2. Mean duration of follow-up was 4.1±3,7 years. At the last visit, median eGFR was 74 (IQR; 43-126) ml/min/1.73m2. A total of 6 patients (28,6%) underwent a renal replacement therapy (RRT), 3 of them died in infancy and 2 of them had renal transplantation during follow up. All patients had bi-allelic PKHD1 mutation. For ADPKD patients, the mean age at diagnosis was 5.5±4.6 years. At the time of diagnosis 11 (22.9%) patients had eGFR&lt;90 ml/min/1.73m2. Mean duration of follow-up was 2,7±2.3 years. At the last visit, median eGFR was 114 (IQR; 98-135) ml/min/1.73m2. Only one patient underwent a renal transplantation. A total of 42 patients (87.5%) had a heterozygous PKD1 mutation while 6 (12.5%) had a heterozygous PKD2 mutation. The rate of growth retardation, hypertension at diagnosis and progression to chronic kidney disease (CKD) were higher in patients with PKHD1 mutation than the patients with PKD1 or PKD2 mutation (p &lt; 0.001, p &lt; 0.001 and p = 0.001, respectively). In kidney survival analysis, mutation type, growth retardation at presentation, increased renal echogenity in ultrasonography were found as independent risk factors for progression to CKD. Conclusion Cystic kidney diseases are one of the most clinically and genetically heterogenous diseases. Differentiating them and establishing the predictors for CKD development is important to provide appropriate management including choosing appropriate donor in renal transplantation.

scholarly journals Hydroureteronephrosis in women with pelvic organ prolapse: a prospective cohort study

2018 ◽  
Vol 7 (9) ◽  
pp. 3664
Author(s):  
Pushplata Kumari ◽  
Emily Divya Ebenezer ◽  
Caroline Salomi ◽  
Vaibhav Londhe ◽  
Aruna Nitin Kekre
Keyword(s):  
Chronic Kidney Disease ◽  
Risk Factor ◽  
Pelvic Organ Prolapse ◽  
Kidney Disease ◽  
Prospective Observational Study ◽  
Surgical Repair ◽  
Significant Risk ◽  
Significant Risk Factor ◽  
Pelvic Organ ◽  
The Mean

Background: Pelvic organ prolapses (POP) is a common problem in women. The prevalence of POP increase with age. The true prevalence and risk factor for developing hydroureteronephrosis (HUN) in women with pelvic organ prolapse is still unclear due to lack of prospective studies on sufficiently large cohorts. This prospective study was done to study the prevalence of HUN in women with POP and to identify the risk factors for developing HUN.Methods: In this prospective observational study 219 patients were recruited for surgical repair for pelvic organ prolapse for 2 years.  Preoperatively, all patients had transabdominal scan to assess the uterus, adnexa and to look for Hydroureteronephrosis (HUN). Women with presence of HUN were followed postoperatively look for the resolution of HUN.Results: The prevalence of bilateral HUN was 6.85%. The mean age of women with HUN ranged from 51-69 years. Diabetes and hypertension were significant risk factor for development of HUN (OR 4.70, 95% CI -1.59-13.88 and OR 3.72, 95% CI- 1.23-11.1 respectively). There was a statistically significant correlation between chronic kidney disease and HUN. (OR 1 with 95%: CI 9.49-30.42). The correlation between stage of pelvic organ prolapse and HUN was not statistically significant (p = 0.062). There was a statistically significant correlation between the duration (2years -15 years) of POP to HUN. (OR 0.233, 95%0.13-0.419). Patients were followed up post operatively for resolution of HUN. HUN resolved in 9 women (60%) and persisted in 6 (40%).Conclusions: The prevalence of bilateral HUN in women with pelvic organ prolapse was 6.8%. Presence of hypertension, diabetes and chronic kidney disease was a risk factor for HUN. HUN resolved in 60% of women after pelvic reconstructive surgery.

Downregulation of Ke 6, a novel gene encoded within the major histocompatibility complex, in murine polycystic kidney disease

1993 ◽  
Vol 13 (3) ◽  
pp. 1847-1853
Author(s):  
N Aziz ◽  
M M Maxwell ◽  
B St Jacques ◽  
B M Brenner
Keyword(s):  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Kidney Diseases ◽  
Chromosome 17 ◽  
Cystic Kidney ◽  
Murine Models ◽  
Polycystic Kidney ◽  
Bacterial Proteins ◽  
Short Chain Alcohol ◽  
Cystic Kidney Diseases

Polycystic kidney disease (PKD) is characterized by progressive enlargement of the kidneys due to numerous expanding cysts ultimately leading to renal failure. We have identified a gene, Ke 6, located within the H-2K/tw5 region on mouse chromosome 17, which is downregulated in two distinct murine models of heritable PKD. Ke 6 is a member of the short-chain alcohol dehydrogenase family and possess remarkable amino acid sequence conservation with several bacterial proteins with oxidoreductase function. The Ke 6 gene gives rise to two transcripts--a 1-kb Ke 6a mRNA which is abundant in kidney and liver tissue and a 1.4-kb Ke 6b mRNA which is found at a moderate level in spleen tissue. We report here the complete nucleotide sequence of Ke 6a cDNA and the expression of the Ke 6 gene in murine models of PKD. The Ke 6 gene may be intimately involved in the manifestation of these cystic kidney diseases.

Cystic Kidney Diseases

2019 ◽  
pp. 373-388
Author(s):  
Fouad T. Chebib ◽  
Vicente E. Torres
Keyword(s):  
Kidney Disease ◽  
Kidney Diseases ◽  
Average Rate ◽  
Cystic Kidney ◽  
Renal Protection ◽  
Clinical Complications ◽  
Kidney Cysts ◽  
Autosomal Dominant Polycystic Kidney ◽  
Stage Renal Disease ◽  
End Stage

Autosomal dominant polycystic kidney disease (ADPKD), the most common monogenic kidney disease, is characterized by relentless development of kidney cysts, hypertension, and eventually end-stage renal disease. The enlargement of the bilateral kidney cysts is gradual throughout the lifetime of the patient until little renal parenchyma is recognizable. At that stage, the average rate of GFR decline is 4.4 to 5.9 mL/min/year. Over the past few years, several advancements in diagnosing, prognosticating, and understanding the pathogenesis of the disease have been made. The natural course of ADPKD makes it an ideal disease to be targeted for renal protection. This chapter discusses various aspects of pathophysiology and molecular pathways and addresses in details the various pharmaceutical and nonpharmaceutical interventions in the journey of prevention of clinical complications of ADPKD.

Inherited renal disease

2021 ◽  
pp. 339-401
Keyword(s):  
Genetic Testing ◽  
Kidney Disease ◽  
Kidney Diseases ◽  
Therapeutic Option ◽  
Genetic Diagnosis ◽  
Cystic Kidney ◽  
Disease Pathogenesis ◽  
Rna Molecules ◽  
Molecular Therapies ◽  
Cystic Kidney Diseases

With the advancement in, and increased availability of, genetic testing and a rapidly growing understanding of the genetic basis of many kidney diseases, it is important that nephrologists understand the rationale, limitations, and implications of making a genetic diagnosis in patients with kidney disease. While most inherited kidney diseases are rare, all nephrologists will encounter patients with genetic forms of kidney disease, particularly the cystic kidney diseases. An understanding of the genotype–phenotype relationships across the different inherited kidney diseases provides the nephrologist with an unprecedented understanding of disease pathogenesis. The evolving use of gene-based and molecular therapies utilizing silencing RNA molecules in kidney diseases are likely to become a growing therapeutic option in the future. Nephrologists will need to understand and embrace these new therapies, particularly for this group of kidney diseases.

scholarly journals CANDESARTAN IN CARDIOLOGY PRACTICE

2017 ◽  
pp. 12-16
Author(s):  
N. A. Dzhaiani
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Chronic Kidney Disease ◽  
Risk Factor ◽  
Heart Disease ◽  
Hemorrhagic Stroke ◽  
Kidney Diseases ◽  
Significant Risk ◽  
Significant Risk Factor ◽  
Ischemic Attack

The most significant risk factor for the development of cardiovascular diseases such as myocardial infarction, ischemic heart disease, chronic heart failure, is arterial hypertension (AH). [1] AH also contributes to the development of cerebrovascular pathology (ischemic or hemorrhagic stroke, transient ischemic attack) and kidney diseases (chronic kidney disease).

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