Patients with kidney disease are at increased maternal and fetal risk during pregnancy. In particular, glomerular-based kidney disease is overrepresented among younger patient populations and is therefore a common form of kidney disease that requires management during pregnancy. Potential untoward outcomes include progression of underlying renal dysfunction, worsening of urine protein excretion and hypertension, and untoward fetal outcomes including intrauterine growth restriction and preterm delivery. However, prognostication of an individual woman’s pregnancy-associated risk in the setting of chronic kidney disease (CKD) remains profoundly challenging, especially in the context of glomerular-based kidney disease, wherein there is often a combination of different
In the past several years, major progress has been made in understanding the mechanisms underlying the development and progression of IgA nephropathy (IgAN). These advances have contributed to the generation of an ever-expanding catalog of measurable variables that provide diagnostic or prognostic information about IgAN. Such measures span the gamut from immune mediators and metabolites detectable in serum or urine, to genetic and epigenetic traits, to histologic features both traditional and novel. IgAN has a complex multistep pathogenesis involving essentially every branch of the immune system, and this progress in measurable variables holds great promise for better characterizing the disease
Membranoproliferative glomerulonephritis (MPGN), also termed mesangiocapillary glomerulonephritis, is a diagnosis based on a glomerular injury pattern common to a heterogeneous group of diseases (1). MPGN is characterized by both an inflammatory (proliferative) and resolving (membrane) phase. Histologically, the proliferative phase is characterized by an increase in mesangial and endocapillary cellularity, and the resolving phase is characterized by an increase in mesangial matrix and capillary wall remodeling with basement membrane material forming a wall, resulting in double contour formation.
Previously, MPGN was classified into MPGN types I, II, and III, based on the ultrastructural location of the electron-dense deposits
Clinicians view kidney disease as a continuum where kidney failure results from a combination of patient susceptibility factors (diabetes, hypertension, or low nephron mass) combined with episodes of kidney injury (acute kidney injury [AKI]). Clinicians use traditional biomarkers such as serum creatinine, urine output, and albumin as indices of kidney function to diagnose, prognosticate, implement therapy, and monitor progression. These traditional biomarkers are far from ideal. Serum creatinine is a surrogate for kidney function, not injury, and often only signals the injury after several days. Creatinine is also a poor surrogate for renal reserve in assessing patients for chronic kidney
The burden of renal disease is continuing to increase not only in the U.S. population but worldwide, as comorbidity factors such as obesity and diabetes become more prevalent (1). This year, the CDC estimates that more than 10 percent of adults in the United States, approximately 20 million people, may have chronic kidney disease (CKD) in varying degrees of severity, with many people being unaware that they either have CKD or are at increased risk of developing it (2).
The prevalence of CKD, now and in the future, truly represents a public health challenge. The area
Cirrhosis is a major contributor to the burden of disease in society, and much of the morbidity and mortality associated with cirrhosis is due to the complications of portal hypertension. Acute kidney injury (AKI) is a frequent complication in patients with cirrhosis, occurring in up to 20 percent of hospitalized patients (1). Despite the high rate of AKI in this patient population, there is often a delay in early diagnosis of AKI. Furthermore, there are clinical challenges in correctly diagnosing the etiology of AKI, which in turn can alter specific therapy. This article will focus on the current
There has been considerable interest in studying novel biomarkers in chronic kidney disease (CKD) beyond the conventional clinical indices, such as serum creatinine, blood urea nitrogen, and urine protein or urine albumin. The motivation for this is similar to what has been outlined in other articles in this issue of ASN Kidney News. For example, novel biomarkers may improve our ability to better risk classify patients and guide clinical actions (e.g., closer follow-up and more intense treatment for patients at higher risk of progression of CKD), to identify high-risk patients for enrollment into clinical trials (as enriched enrollment
Contrast-induced acute kidney injury (CI-AKI) is a common condition that is associated with serious, adverse short- and long-term outcomes. Despite substantial advancements in our understanding of CI-AKI, the capacity to effectively risk-stratify patients, diagnose incipient renal injury before elevations in serum creatinine (SCr) manifest, and identify patients at highest risk for adverse downstream events is limited. Blood and urine biomarkers of kidney injury hold promise as a means by which the risk-stratification, diagnosis, and prediction of prognosis of CI-AKI could be significantly enhanced, and the judicious implementation of cost-effective preventive care and treatment to mitigate adverse outcomes substantially improved.
The search for biomarkers in body fluids is evolving into a broader quest for molecular phenotyping of tissue and disease reclassification. The original biomarker concept was too limited, failing to recognize that the interpretation of the molecular changes in body fluids requires a molecular understanding of the diseased tissue.
A molecular biomarker in nephrology implies a molecule that can be measured in body fluids as an indicator of a pathologic state in kidney tissue, perhaps avoiding biopsies by providing similar information. This demands that the biomarker is superior to current laboratory assessments such as creatinine
Renal insufficiency is prevalent and clinically relevant in the setting of congestive heart failure. When admitted for acute decompensation, on average 1 out of 5 patients has a rise in serum creatinine, 1 out of 10 requires some form of dialysis, and 1 out of 20 requires long-term renal replacement therapies (1). These startling observations highlight the fact that adequate renal function plays a pivotal role in the clinical stability of heart failure. Hence, the term “cardio-renal syndrome” (CRS) has been coined to describe the extreme of cardio-renal dysregulation whereby therapy to relieve congestive symptoms of heart failure