scholarly journals Acute Kidney Injury in ADPKD Patients with Pneumonia

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Carlos Franco Palacios ◽  
Mira T. Keddis ◽  
Dingxin Qin ◽  
Ladan Zand ◽  
Guangxi Li ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Autosomal Dominant ◽  
Kidney Injury ◽  
Polycystic Kidney ◽  
X Ray ◽  
Lower Baseline ◽  
Acute Pneumonia ◽  
Chest X Ray ◽  
Hospital Stays ◽  
Autosomal Dominant Polycystic Kidney

Background. In animal models, polycystic kidneys are susceptible to acute kidney injury (AKI). We examined the occurrence of AKI in a cohort of autosomal dominant polycystic kidney disease (ADPKD) and non-ADPKD patients with acute pneumonia.Design. All ADPKD patients admitted to Mayo Clinic Rochester for pneumonia from January 1990 to April 2010 were examined. Sixty-three patients had lobar infiltration and consolidation on chest X-ray. After excluding patients on dialysis, with organ transplantation, and on chronic immunosuppression, 24 remaining ADPKD patients were enrolled. Twenty-three of the 24 were matched with 92 (1 : 4 ratio) non-ADPKD pneumonia patients based on their baseline eGFR. AKI was defined as serum creatinine elevation ≥0.3 mg/dL.Results. Sixteen of the 23 ADPKD patients (69.6%) and 36 of the 92 (39.1%) non-ADPKD patients developed AKI,P=0.008. In both groups, those who developed AKI had a lower baseline eGFR (41.1±5.00versus58.7±11.8in ADPKD and40.2±3.65versus51.8±2.24 mL/min/1.73 m2in the non-ADPKD group), more intensive care unit admissions, and longer hospital stays. AKI was associated with a reduced survival in both groups.Conclusions. Patients with ADPKD admitted for acute pneumonia had more frequent episodes of AKI than non-ADPKD patients with comparable kidney function.

scholarly journals Metformin Improves Relevant Disease Parameters in an Autosomal Dominant Polycystic Kidney Disease Mouse Model

2021 ◽  
Author(s):  
Nuria M Pastor-Soler ◽  
Hui Li ◽  
Jessica Pham ◽  
Daniel Rivera ◽  
Pei-Yin Ho ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Mouse Model ◽  
Polycystic Kidney Disease ◽  
Autosomal Dominant ◽  
Severe Disease ◽  
Treatment Options ◽  
Kidney Injury ◽  
Polycystic Kidney ◽  
Gene And Protein Expression ◽  
Autosomal Dominant Polycystic Kidney

Autosomal dominant polycystic kidney disease (ADPKD), caused by mutations in the PKD1 or PKD2 genes encoding polycystins, presents with progressive development of kidney cysts and eventual end-stage kidney disease (ESKD) with limited treatment options. Previous work showed that metformin reduces cyst growth in rapid ADPKD mouse models via inhibition of CFTR-mediated fluid secretion, mTOR, and cAMP pathways. The present study importantly tested the effectiveness of metformin as a therapy for ADPKD in a more clinically relevant Pkd1RC/RC mouse model, homozygous for the R3277C knock-in point mutation in the Pkd1 gene. This mutation causes ADPKD in humans. Pkd1RC/RC male and female mice, which have slow progression to ESKD, received metformin (300 mg/kg/day in drinking water vs. water alone) from 3 to 9 or 12 months of age. As previously reported, Pkd1RC/RC females had a more severe disease phenotype than males. Metformin treatment reduced the ratio of total kidney weight to body weight relative to age- and sex-matched untreated controls at both 9 and 12 months and reduced cystic index in females at 9 months. Metformin also increased glomerular filtration rate (GFR), lowered systolic blood pressure, improved anemia, and lowered blood urea nitrogen levels relative to controls in both sexes. Moreover, metformin reduced gene expression of key inflammatory markers and both gene and protein expression of kidney injury marker-1 and cyclin-dependent kinase-1 vs. untreated controls. Altogether, these findings suggest several beneficial effects of metformin in this highly relevant slowly progressive ADPKD mouse model, which may help inform new ADPKD therapies in patients.

scholarly journals Association between urinary biomarkers and disease progression in adults with autosomal dominant polycystic kidney disease

2019 ◽  
Vol 13 (4) ◽  
pp. 607-612
Author(s):  
Alfons Segarra-Medrano ◽  
Marisa Martin ◽  
Irene Agraz ◽  
Mercè Vilaprinyó ◽  
Betty Chamoun ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Kidney Function ◽  
Autosomal Dominant ◽  
Kidney Injury ◽  
Polycystic Kidney ◽  
Β2 Microglobulin ◽  
Urinary Levels ◽  
Autosomal Dominant Polycystic Kidney ◽  
Egfr Slope

Abstract Background Height-adjusted total kidney volume (htTKV) is considered as the best predictor of kidney function in patients with autosomal dominant polycystic kidney disease (ADPKD), but its limited predictive capacity stresses the need to find new biomarkers of ADPKD progression. The aim of this study was to investigate urinary biomarkers of ADPKD progression. Methods This observational study included ADPKD patients, and two comparator groups of ischaemic and non-ischaemic kidney injury: benign nephroangiosclerosis patients and non-ischaemic chronic kidney disease (CKD) patients. Proteinuria, htTKV and urinary levels of molecules are associated with ischaemia and/or tubular injury. The slope of estimated glomerular filtration rate (eGFR) was used as a dependent variable in univariate and multivariate models of kidney function decline. Results The study included 130 patients with ADPKD, 55 with nephroangiosclerosis and 40 with non-ischaemic CKD. All patients had increased urinary concentrations of biomarkers associated with tubular lesions (liver fatty acid-binding protein, kidney injury molecule-1, β2-microglobulin) and molecules overexpressed under ischaemic conditions [hypoxia-inducible factor-1α, vascular endothelial growth factor (VEGF) and monocyte chemoattractant protein-1 (MCP-1)]. These biomarkers correlated positively with htTKV and negatively with the eGFR slope. htTKV was the single best predictor of the eGFR slope variability in univariate analyses. However, a multivariate model including urinary levels of β2-microglobulin, MCP-1 and VEGF improved the capacity to predict the decline of eGFR in ADPKD patients compared with htTKV alone. Conclusions The urinary levels of molecules associated with either renal ischaemia (VEGF and MCP-1) or tubular damage (β2-microglobulin) are associated with renal function deterioration in ADPKD patients, and are, therefore, candidates as biomarkers of ADPKD progression.

scholarly journals Hypercalcemia, Anemia, and Acute Kidney Injury: A Rare Presentation of Sarcoidosis

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Neeraj Sharma ◽  
Hassan Tariq ◽  
Kalpana Uday ◽  
Yevgeniy Skaradinskiy ◽  
Masooma Niazi ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Hematologic Malignancy ◽  
Granulomatous Inflammation ◽  
Kidney Injury ◽  
Transbronchial Biopsy ◽  
Rare Presentation ◽  
X Ray ◽  
Initial Impression ◽  
Chest X Ray ◽  
Noncontrast Computed Tomography

We discuss a case of a 61-year-old woman who presented with substernal chest pain. She was found to have elevated calcium levels, anemia, and acute kidney injury. The hypercalcemia persisted despite therapy with fluids and bisphosphonates. She was found to have nonparathyroid hormone (PTH) mediated hypercalcemia. The chest X-ray did not reveal any pathology. Our Initial impression was likely underlying hematologic malignancy such as lymphoma or multiple myeloma. A bone marrow biopsy was performed that revealed nonnecrotizing granulomatous inflammation. Further workup revealed elevated vitamin 1,25 dihydroxy level, beta-two microglobulin level, and ACE levels. Noncontrast computed tomography (CT) scan of chest showed bilateral apical bronchiectasis, but did not show any lymphadenopathy or evidence of malignancy. Subsequently, a fiber optic bronchoscopy with transbronchial biopsy showed nonnecrotizing granulomatous inflammation consistent with sarcoidosis. After initiating glucocorticoid therapy, the patient’s hypercalcemia improved and her kidney function returned to baseline.

scholarly journals Calcium Signaling Mediates Cell Death and Crosstalk with Autophagy in Kidney Disease

Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 3204
Author(s):  
Bo Ning ◽  
Chuanzhi Guo ◽  
Anqi Kong ◽  
Kongdong Li ◽  
Yimin Xie ◽  
...  
Keyword(s):  
Cell Death ◽  
Kidney Disease ◽  
Autosomal Dominant ◽  
Kidney Diseases ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
The Body ◽  
Polycystic Kidney ◽  
Progression Of Kidney Disease ◽  
Autosomal Dominant Polycystic Kidney

The kidney is an important organ for the maintenance of Ca2+ homeostasis in the body. However, disruption of Ca2+ homeostasis will cause a series of kidney diseases, such as acute kidney injury (AKI), chronic kidney disease (CKD), renal ischemia/reperfusion (I/R) injury, autosomal dominant polycystic kidney disease (ADPKD), podocytopathy, and diabetic nephropathy. During the progression of kidney disease, Ca2+ signaling plays key roles in various cell activities such as necrosis, apoptosis, eryptosis and autophagy. Importantly, there are complex Ca2+ flux networks between the endoplasmic reticulum (ER), mitochondria and lysosomes which regulate intracellular Ca2+ signaling in renal cells and contribute to kidney disease. In addition, Ca2+ signaling also links the crosstalk between various cell deaths and autophagy under the stress of heavy metals or high glucose. In this regard, we present a review of Ca2+ signaling in cell death and crosstalk with autophagy and its potential as a therapeutic target for the development of new and efficient drugs against kidney diseases.

Kidney injury molecule-1 expression in murine polycystic kidney disease

2002 ◽  
Vol 283 (6) ◽  
pp. F1326-F1336 ◽  
Author(s):  
E. Wolfgang Kuehn ◽  
Kwon Moo Park ◽  
Stefan Somlo ◽  
Joseph V. Bonventre
Keyword(s):  
Kidney Disease ◽  
Mouse Model ◽  
Polycystic Kidney Disease ◽  
Autosomal Dominant ◽  
Interstitial Fibrosis ◽  
Kidney Injury ◽  
Polycystic Kidney ◽  
Tubular Cells ◽  
Autosomal Dominant Polycystic Kidney ◽  
Kidney Injury Molecule 1

Kidney injury molecule-1 (Kim-1) is a type 1 membrane protein maximally upregulated in proliferating and dedifferentiated tubular cells after renal ischemia. Because epithelial dedifferentiation, proliferation, and local ischemia may play a role in the pathophysiology of autosomal dominant polycystic kidney disease, we investigated Kim-1 expression in a mouse model of this disease. In the Pkd2WS25/− mouse model for autosomal dominant polycystic kidney disease, cystic kidneys show markedly upregulated Kim-1 levels compared with noncystic control kidneys. Kim-1 is present in a subset of cysts of different sizes and segmental origins and in clusters of proximal tubules near cysts. Kim-1-expressing tubular cells show decreased complexity and quantity of basolateral staining for Na-K-ATPase. Other changes in polarity characteristic of ischemic injury are not present in Kim-1-expressing pericystic tubules. Polycystin-2 expression is preserved in Kim-1-expressing tubules. The interstitium surrounding Kim-1-expressing tubules shows high proliferative activity and staining for smooth muscle α-actin, characteristic of myofibroblasts. Although the functional role of the protein in cysts remains unknown, Kim-1 expression in tubules is strongly associated with partial dedifferentiation of epithelial cells and may play a role in the development of interstitial fibrosis.

scholarly journals Metastatic Pulmonary Calcification in a Hemodialysis Patient after Renal Transplantation

2021 ◽  
Vol 8 (2) ◽  
Author(s):  
Vicente R ◽  
◽  
Santos R ◽  
Amoedo M ◽  
◽  
...  
Keyword(s):  
Renal Transplantation ◽  
Autosomal Dominant ◽  
Hemodialysis Patient ◽  
Left Lung ◽  
Polycystic Kidney ◽  
X Ray ◽  
Acute Vascular Rejection ◽  
Slow Progression ◽  
Autosomal Dominant Polycystic Kidney ◽  
Metastatic Pulmonary Calcification

This is the case of a 64-year-old man, on renal replacement therapy since 2008, due to autosomal dominant polycystic kidney disease. The patient was on peritoneal dialysis from 2008 to 2016, when he underwent renal transplantation. Transplant duration was less than a month due to acute vascular rejection. Since then, he is on hemodialysis. A few months after transplantation, it was incidentally identified confluent bilateral opacities, more prominent on the left lung in a routine X-ray (Figure 1). The patient had made a chest radiography in 2015 without any changes at that time. The CT scan showed parenchymatous densification areas, partially calcified, in both lungs (Figure 2). The patient also developed secondary hyperparathyroidism refractory to medical therapy but refused surgery. Nevertheless, the lesions had a slow progression until the present time.

Sign in / Sign up

Export Citation Format

Share Document