scholarly journals Advances in the Pathology of Glomerular Diseases

2013 ◽  
pp. 12-21 ◽  
Author(s):  
Jan J. Weening ◽  
Pierre Ronco ◽  
Giuseppe Remuzzi
Keyword(s):  
Glomerular Diseases

Urinary Cytokines as Biomarkers in Glomerular Diseases

2016 ◽  
Vol 5 (2) ◽  
pp. 71-80 ◽  
Author(s):  
Maria J. Stangou ◽  
Aikaterini Papagianni
Keyword(s):  
Glomerular Diseases

scholarly journals Renal Complications Related to Checkpoint Inhibitors: Diagnostic and Therapeutic Strategies

Diagnostics ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 1187
Author(s):  
Julie Belliere ◽  
Julien Mazieres ◽  
Nicolas Meyer ◽  
Leila Chebane ◽  
Fabien Despas
Keyword(s):  
Checkpoint Inhibitors ◽  
Treatment Strategies ◽  
Kidney Injury ◽  
Immunosuppressive Drugs ◽  
Peripheral Tolerance ◽  
Electrolyte Disorders ◽  
Glomerular Diseases ◽  
Renal Complications ◽  
Lower Baseline ◽  
Low Incidence

Immune checkpoint inhibitors (ICI) targeting CTLA-4 and the PD-1/PD-L1 axis have unprecedentedly improved global prognosis in several types of cancers. However, they are associated with the occurrence of immune-related adverse events. Despite their low incidence, renal complications can interfere with the oncologic strategy. The breaking of peripheral tolerance and the emergence of auto- or drug-reactive T-cells are the main pathophysiological hypotheses to explain renal complications after ICI exposure. ICIs can induce a large spectrum of renal symptoms with variable severity (from isolated electrolyte disorders to dialysis-dependent acute kidney injury (AKI)) and presentation (acute tubule-interstitial nephritis in >90% of cases and a minority of glomerular diseases). In this review, the current trends in diagnosis and treatment strategies are summarized. The diagnosis of ICI-related renal complications requires special steps to avoid confounding factors, identify known risk factors (lower baseline estimated glomerular filtration rate, proton pump inhibitor use, and combination ICI therapy), and prove ICI causality, even after long-term exposure (weeks to months). A kidney biopsy should be performed as soon as possible. The treatment strategies rely on ICI discontinuation as well as co-medications, corticosteroids for 2 months, and tailored immunosuppressive drugs when renal response is not achieved.

Understanding glomerular diseases through proteomics

2021 ◽  
pp. 1-21
Author(s):  
E. Mavrogeorgis ◽  
H. Mischak ◽  
J. Beige ◽  
A. Latosinska ◽  
J. Siwy
Keyword(s):  
Glomerular Diseases

P0234LOW URINARY CITRATE LEVELS ARE NOT SPECIFIC OF AUTOSOMAL POLYCYSTIC KIDNEY DISEASE (ADPKD) AND ARE PRESENT WHEN RENAL FUNCTION IS IMPAIRED IN ALL NEPHROPATIES

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Francisco-Jose Borrego-Utiel ◽  
Enoc Merino Garcia ◽  
Isidoro Herrera ◽  
Clara Moriana Dominguez ◽  
Victoria Camacho Reina ◽  
...  
Keyword(s):  
Renal Function ◽  
Uric Acid ◽  
Kidney Disease ◽  
Renal Impairment ◽  
Polycystic Kidney Disease ◽  
Normal Renal Function ◽  
Serum Bicarbonate ◽  
Polycystic Kidney ◽  
Glomerular Diseases ◽  
Urinary Citrate

Abstract Background and Aims In polycystic kidney disease (PKD) it is frequently found a reduction in urinary citrate that is related with degree of renal impairment but it is unknown if this alteration is specific or if it is also present in other nephropathies. Recently it has been suggested that urinary citrate could be a marker of covert metabolic acidosis and reflects acid retention in chronic kidney disease (CKD). Our aim was to compare urinary citrate in PKD with other renal diseases and to show its relation with serum bicarbonate and excretion of uric acid and calcium. Method We determined citrate, calcium and uric acid in 24-hour urine in patients with PKD and with other nephropathies with varied degree of renal impairment followed in a outpatient clinic of nephrology. Results We included 291 patients, 119 with glomerular diseases, 116 with PKD, 21 with other nephropathies, and 35 patients with normal renal function. Urinary citrate was higher in women (Females 309±251 mg/gCr vs. males 181±145 mg/gCr, p<0.001) and in patients with normal renal function (normal 380±210 mg/gCr; PKD 203±166 mg/gCr; glomerular 279±282 mg/gCr; p<0,001). PKD patients showed similar values of urinary citrate to patients with glomerular diseases and with other nephropathies. We observed a progressive reduction in urinary citrate parallel to degree of renal impairment, in a comparable way among patients with PKD and glomerular diseases. We did not observe a relationship between urinary citrate and serum bicarbonate levels. Calcium and uric acid elimination in ADPKD patients was similar to other nephropathies and lower to patients with normal renal function. However, serum uric acid was significantly higher in glomerular patients than other nephropathies after adjust with glomerular filtration rate and sex. Conclusion Hypocitraturia is not specific of PKD but it is also present in all nephropathies. Urinary citrate are related to degree of renal impairment and it is not related with serum bicarbonate. We think that it could be interesting to study urinary citrate as a marker of renal function and its role as prognostic factor of renal deterioration.

scholarly journals Podocyte injury: the role of proteinuria, urinary plasminogen, and oxidative stress

2016 ◽  
Vol 311 (6) ◽  
pp. F1308-F1317 ◽  
Author(s):  
Leopoldo Raij ◽  
Runxia Tian ◽  
Jenny S. Wong ◽  
John C. He ◽  
Kirk N. Campbell
Keyword(s):  
Oxidative Stress ◽  
Glomerular Filtration ◽  
Biologically Active ◽  
Current Evidence ◽  
Glomerular Sclerosis ◽  
Glomerular Diseases ◽  
Podocyte Injury ◽  
Filtration Barrier ◽  
Focal Segmental Glomerular Sclerosis

Podocytes are the key target for injury in proteinuric glomerular diseases that result in podocyte loss, progressive focal segmental glomerular sclerosis (FSGS), and renal failure. Current evidence suggests that the initiation of podocyte injury and associated proteinuria can be separated from factors that drive and maintain these pathogenic processes leading to FSGS. In nephrotic urine aberrant glomerular filtration of plasminogen (Plg) is activated to the biologically active serine protease plasmin by urokinase-type plasminogen activator (uPA). In vivo inhibition of uPA mitigates Plg activation and development of FSGS in several proteinuric models of renal disease including 5/6 nephrectomy. Here, we show that Plg is markedly increased in the urine in two murine models of proteinuric kidney disease associated with podocyte injury: Tg26 HIV-associated nephropathy and the Cd2ap −/− model of FSGS. We show that human podocytes express uPA and three Plg receptors: uPAR, tPA, and Plg-RKT. We demonstrate that Plg treatment of podocytes specifically upregulates NADPH oxidase isoforms NOX2/NOX4 and increases production of mitochondrial-dependent superoxide anion (O2−) that promotes endothelin-1 synthesis. Plg via O2− also promotes expression of the B scavenger receptor CD36 and subsequent increased intracellular cholesterol uptake resulting in podocyte apoptosis. Taken together, our findings suggest that following disruption of the glomerular filtration barrier at the onset of proteinuric disease, podocytes are exposed to Plg resulting in further injury mediated by oxidative stress. We suggest that chronic exposure to Plg could serve as a “second hit” in glomerular disease and that Plg is potentially an attractive target for therapeutic intervention.

Progression of Renal Failure in Chronic Primary Glomerular Diseases

Nephron ◽  
1994 ◽  
Vol 68 (1) ◽  
pp. 32-37 ◽  
Author(s):  
Ana Gonzalo ◽  
Araceli Gallego ◽  
Maite Rivera ◽  
Nieves Gallego ◽  
Joaquín Ortuño
Keyword(s):  
Renal Failure ◽  
Glomerular Diseases ◽  
Progression Of Renal Failure ◽  
Primary Glomerular Diseases

scholarly journals In situ evaluation of podocin in normal and glomerular diseases

2003 ◽  
Vol 64 (6) ◽  
pp. 2092-2099 ◽  
Author(s):  
Izumi Horinouchi ◽  
Hitoshi Nakazato ◽  
Tomoyasu Kawano ◽  
Ken-Ichi Iyama ◽  
Akio Furuse ◽  
...  
Keyword(s):  
Glomerular Diseases

scholarly journals Onco-Nephrology: Glomerular Diseases with Cancer

2012 ◽  
Vol 7 (10) ◽  
pp. 1701-1712 ◽  
Author(s):  
Jean-François Cambier ◽  
Pierre Ronco
Keyword(s):  
Glomerular Diseases
Sign in / Sign up

Export Citation Format

Share Document