Alteration of the gut microbiota by vinegar is associated with amelioration of hyperoxaluria-induced kidney injury

Abstract Context.—Many new therapies have emerged within the last 5 to 10 years to treat a variety of conditions. Several of these have direct or indirect renal toxicities that may go undiagnosed without careful attention of the pathologist to a patient's clinical history, particularly the addition of new medications or treatments. Objective.—To discuss patterns of renal injury resulting from medications or therapeutic regimens that have been introduced within the last 10 years. Recognition of these patterns may allow the pathologist to alert the attending clinician to a possible drug-induced renal injury and prevent further deterioration of renal function and possible chronic kidney disease. Data Sources.—A review of recent literature and unpublished observations of case-derived material. Conclusions.—A number of newer therapies have emerged as agents of renal toxicity, producing a variety of pathologic changes in the kidney. The outcome can be acute or chronic glomerular, tubular, interstitial, and/or vascular injury. Some drugs will result in irreversible changes and end-stage renal disease, whereas many of the alterations can be reversed with removal of the offending agent, avoiding potential long-term kidney injury.

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Congenital abnormalities of the kidneys and urinary tract

Paediatric Nephrology ◽

10.1093/med/9780198784272.003.0003 ◽

2019 ◽

pp. 57-86

Author(s):

Lesley Rees ◽

Nicholas J.A Webb ◽

Detlef Bockenhauer ◽

Marilynn G. Punaro

Keyword(s):

Urinary Tract Infection ◽

Urinary Tract ◽

Kidney Disease ◽

Tract Infection ◽

Renal Injury ◽

Incidental Findings ◽

Renal Damage ◽

Congenital Abnormalities ◽

End Stage Kidney Disease ◽

End Stage

Congenital abnormalities of the kidneys and urinary tract (CAKUT) are the commonest cause of renal problems in children, ranging from asymptomatic or incidental findings to a cause of urinary tract infection and obstruction, renal damage, and end-stage kidney disease. The investigation and management of CAKUT depend on the potential for causing renal injury.

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Troponins, Acute Coronary Syndrome and Renal Disease: From Acute Kidney Injury Through End-stage Kidney Disease

European Cardiology Review ◽

10.15420/ecr.2019.28.2 ◽

2019 ◽

Vol 14 (3) ◽

pp. 187-190

Author(s):

Debasish Banerjee ◽

Charlotte Perrett ◽

Anita Banerjee

Keyword(s):

Acute Kidney Injury ◽

Kidney Disease ◽

Kidney Diseases ◽

Kidney Injury ◽

Left Ventricular ◽

End Stage Kidney Disease ◽

Chronic Kidney Diseases ◽

Coronary Syndrome ◽

End Stage ◽

Cardiac Troponins

The diagnosis of acute coronary syndromes (ACS) is heavily dependent on cardiac biomarker assays, particularly cardiac troponins. ACS, particularly non-ST segment elevation MI, are more common in patients with acute kidney injury, chronic kidney disease (CKD) and end-stage kidney disease (ESKD), are associated with worse outcomes than in patients without kidney disease and are often difficult to diagnose and treat. Hence, early accurate diagnosis of ACS in kidney disease patients is important using easily available tools, such as cardiac troponins. However, the diagnostic reliability of cardiac troponins has been suboptimal in patients with kidney disease due to possible decreased clearance of troponin with acute and chronic kidney impairment and low levels of troponin secretion due to concomitant cardiac muscle injury related to left ventricular hypertrophy, inflammation and fibrosis. This article reviews the metabolism and utility of cardiac biomarkers in patients with acute and chronic kidney diseases. Cardiac troponins are small peptides that accumulate in both acute and chronic kidney diseases due to impaired excretion. Hence, troponin concentrations rise and fall with acute kidney injury and its recovery, limiting their use in the diagnosis of ACS. Troponin concentrations are chronically elevated in CKD and ESKD, are associated with poor prognosis and decrease the sensitivity and specificity for diagnosis of ACS. Yet, the evidence indicates that the use of high-sensitivity troponins can confirm or exclude a diagnosis of ACS in the emergency room in a significant proportion of kidney disease patients; those patients in whom the results are equivocal may need longer in-hospital assessment.

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Long-term outcomes following vehicle trauma related acute kidney injury requiring renal replacement therapy: A nationwide population study

10.21203/rs.2.23346/v1 ◽

2020 ◽

Author(s):

Chieh-Kai Chan ◽

John R Prowle ◽

Vin-Cent Wu

Keyword(s):

Acute Kidney Injury ◽

Renal Replacement Therapy ◽

Kidney Disease ◽

Replacement Therapy ◽

Kidney Injury ◽

Long Term Outcomes ◽

End Stage Kidney Disease ◽

End Stage ◽

Long Term Mortality

Abstract Background Acute kidney injury (AKI) is a frequent complication of traumatic injury; however, long-term outcomes such as mortality and end-stage kidney disease (ESKD) have been rarely reported in this important patient population. We compared the long-term outcome of traumatic and non-traumatic AKI requiring renal replacement therapy (AKI-RRT). Methods This nationwide cohort study used data from the Taiwan National Health Insurance Research Database. Vehicle-trauma patients developing AKI-RRT during hospitalization were identified, and matching non-traumatic AKI-RRT patients were identified between 2000 and 2010. The incidences of end-stage kidney disease (ESKD), 30-day, and long-term mortality were evaluated, and clinical and demographic associations with these outcomes were identified using Cox proportional hazards regression models. Results 546 traumatic AKI-RRT patients, median age 47.6 years (interquartile range: 29.0-64.3) and 76.4% male, were identified. Compared to non-traumatic AKI-RRT, traumatic AKI-RRT patients had longer length of stay in hospital [median (IQR):15 (5-34) days vs 6 (3-11) days; p < 0.001). After propensity matching with non-traumatic AKI-RRT cases with similar demographic and clinical characteristics. Traumatic AKI-RRT patients had lower rates of long-term mortality (adjusted hazard ratio (HR), 0.488; 95% CI, 0.405-0.588; p < 0.001), but similar rates of ESKD (HR, 1.075; 95% CI, 0.767–1.509; p = 0.674) and short-term risk of death (HR, 1.165; 95% CI, 0.920-1.476; p = 0.205) as non-traumatic AKI-RRT patients. Conclusions Despite severe injuries, traumatic AKI-RRT patients had better long-term survival than non-traumatic AKI-RRT patients, but a similar risk of ESKD. Our results provide a better understanding of long-term outcomes after traumatic AKI-RRT.

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Long-Term Therapeutic Plasma Exchange to Prevent End-Stage Kidney Disease in Adult Severe Resistant Henoch-Schonlein Purpura Nephritis

Case Reports in Nephrology ◽

10.1155/2015/269895 ◽

2015 ◽

Vol 2015 ◽

pp. 1-5

Author(s):

Patrick Hamilton ◽

Olumide Ogundare ◽

Ammar Raza ◽

Arvind Ponnusamy ◽

Julie Gorton ◽

...

Keyword(s):

Renal Function ◽

Kidney Disease ◽

Plasma Exchange ◽

Kidney Injury ◽

Term Treatment ◽

Therapeutic Plasma Exchange ◽

End Stage Kidney Disease ◽

Long Term Treatment ◽

End Stage

A 27-year-old man presented with a palpable purpuric skin rash and joint and abdominal pain in April 2010. He had acute kidney injury and his creatinine quickly deteriorated to 687 μmol/L, with associated nephrotic range proteinuria. Kidney biopsy showed crescentic Henoch-Schonlein nephritis. He was treated with intravenous cyclophosphamide and prednisolone despite which his renal function deteriorated; he required haemodialysis for a short duration and seven sessions of therapeutic plasma exchange (TPE). Renal function improved, but after discharge from hospital he suffered 2 further relapses, each with AKI, in 4 months. Cyclophosphamide was not effective and therefore Rituximab was introduced. He initially had a partial response but his renal function deteriorated despite continued therapy. TPE was the only treatment that prevented rapid renal functional deterioration. A novel long-term treatment strategy involving regular TPE every one to two weeks was initiated. This helped to slow his progression to end-stage kidney disease over a 3-year period and to prolong the need for renal replacement therapy over this time.

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