Membranoproliferative glomerulonephritis MPGN is a type of immune mediated glomerular disease. The name is an indication of its pathology, with thickening of the basement membrane and proliferative changes. Students should be familiar with an overview of this condition, including its pathological features that set it apart from other glomerular disorders, as well as the diagnostic approach and management of MPGN.
Its main function is to reabsorb salt and water, organic solutes like sugar and amino acids, potassium, urea, and phosphate. It also secretes ammonium in the urine. These are kidney diseases that involve structures outside the glomerulus. The causative agents incite a hypersensitivity reaction that leads to an inflammatory infiltrate seeding into the kidneys interstitium and irreversible features of fibrosis and sclerosis.
This leads to the diseases presenting as an acute kidney injury that may end up as an end stage renal disease. Management is per the acute renal injury algorithms that advocate for identification of the inciting agent and its discontinuation alongside watching out for end stage renal disease and timely institution of renal replacement therapy. The kidneys are paired retroperitoneal organs that weigh about grams each.
Each kidney is lined by fibrous capsule for protection. Diabetic Glomerulopathy — Pathogenesis and Management. Diabetic glomerulopathy is the leading cause of chronic renal failure in adults. Long-standing type 1 or type 2 diabetes mellitus is associated with this microvascular complication, along with peripheral neuropathy and retinopathy. The pathology of diabetic glomerulopathy is distinguishable based on certain features, including the presence of pathognomonic Kimmelstiel-Wilson nodules, hence the term Kimmelstiel-Wilson disease.
Students should be aware about this important complication of diabetes, including its pathology, pathophysiology, clinical course and management. Unilateral agenesis is defined as the complete absence of development of one kidney and ureter. The condition is usually silent and is usually detected on fetal ultrasound scan by the presence of empty renal fossa. The incidence of URA is relatively common and is due to genetic as well as maternal causes. Human renal development is initiated by the 5th week of gestation and renal agenesis occurs when the ureteric bud fails to form the ureter, the renal pelvis, and renal mesenchyme.
URA is often associated with anomalies of the contralateral kidney and ureter as well. In this article, you will gain a perfect overview of the distal convoluted tubule, the portion of the nephron of the kidney extending from the loop of Henle up to the collecting duct system. Furthermore, you will learn about the pathophysiology and treatment of the autosomal recessive disorders called Gitelman syndrome and Bartter syndrome for the perfect medical exam preparation.
Potter's Syndrome — Causes and Prognosis. Potter syndrome, also known as the Potter sequence refers to the specific appearance of the baby due to oligohydramnios which is a decrease in amniotic fluid volume which causes deformities in the fetus while in the uterus. These deformities include flattened nasal bridge, epicanthal folds, low set ears and bowed legs. It also leads to pulmonary hypoplasia. The cause has decreased the production of amniotic fluid which is required to cushion the baby against the uterine walls. In this article, we will talk about the microscopic anatomy part of the kidney known as the collecting duct system.
The collecting duct system consists of a series of tubules and ducts that connect the nephrons to a minor calyx or to the renal pelvis. Load more. Renal Pharmacology 13 articles 13 free. Renal Pharmacology 29 quiz questions 16 free. Introduction to Renal Pathology 3 articles 3 free. Introduction to Renal Pathology 12 quiz questions 0 free. Renal Diagnostics 4 articles 4 free. Renal Diagnostics 63 quiz questions 12 free. Diseases of the Nephron 4 articles 4 free. Diseases of the Nephron quiz questions 29 free.
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Glomerulonephritis 81 quiz questions 8 free. Nephrogenic Diabetes Insipidus DI 1 article 1 free. Nephrogenic Diabetes Insipidus DI 23 quiz questions 4 free. SIADH 1 article 1 free. SIADH 16 quiz questions 4 free. Nephrolithiasis 1 article 1 free. Nephrolithiasis 14 quiz questions 3 free. Pravin Shukle, MD Dr. September for Tubulointerstitial Pathology. By Admitere B. June for Rapidly Progressive Crescentic Glomerulonephritis. Ugly way of explaining. Weird pronounciation. By Ismael Francisco V.
June for Glomerulonephritis. By Roja s. By Alfredo H. May for Pathophysiology of Renal Failure. By Romina G. May for Renin-Angiotensin-Aldosterone-System. By Robson M. April for Tubulointerstitial Diseases. April for Introduction to Renal Blood Flow. By Niamh D. March for Lines of Therapy — Drugs in Hypertension.
By Oddom M. January for Fluid and Electrolyte Balance. By Dinesh K. January for Tubulointerstitial Diseases. December for Fluid and Electrolyte Balance. By Neuer N. November for Diuretics — Drugs in Hypertension. Certainly one of the best explanations one could get on this topic!
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By deja A. By Andrei V. By Carmen V. December for Introduction to Renal Blood Flow. By Aws A. November for Fluid and Electrolyte Balance. Lecturio is a must, if you must excel in medical science without sweat! By Olugbemiga J. Cocise, engaging, high learnability index. By Nnamno E. November for Algorithm of Acute Renal Injury. By Gustavo S. Top quality teaching, top quality humour! By Ricardo V. By Tracey H. October for Diseases of the Nephron. By Bjarni J. By Eunbi C. September for Vasodilators — Drugs in Hypertension.
By Nichole C. September for Diseases of the Nephron. Great videos.. By Tayssir Z. September for Fluid and Electrolyte Balance. By Freddie N. August for Fluid and Electrolyte Balance. By aibi y. August for Dehydration: Hypertonic Fluid Disorders. By Mohammed s. In turn, patients with end-stage renal disease are dependent on renal replacement therapy, including kidney transplantation or haemodialysis, for survival.
However, kidney transplantation has been limited by a shortage of donor kidneys, whereas haemodialysis requires high costs relative to the increase in quality of life and average life expectancy. In this scenario, stem cell-based therapies bear the potential to overcome the above-mentioned limitations, providing not only a cost-effective, but also a long-term treatment option for patients with CKD. For kidney disease, three major strategies for stem cell-based therapies have been proposed Figure 1.
The first strategy takes advantage of the anti-fibrotic, anti-inflammatory, and angiogenic potency of MSC, while the second strategy focusses on the transplantation of kidney-specific progenitor cells differentiated from PSC. The third strategy encompasses the xenotransplantation of animal-derived kidneys. In this review, the current status of these three strategies for stem cell-based therapies to confront kidney failure is summarised. The growing concept of kidney resident stem cells, a pre-existing intratubular stem cell population, also referred to as scattered tubular cells, for kidney regeneration is not included in this review.
This cell population has been extensively reviewed elsewhere. Figure 1: Overview of stem cell-based strategies to treat kidney disease. Strategies proposed for renal regeneration include the transplantation of mesenchymal stem cells, nephron progenitor cells derived from pluripotent stem cells, and xenotransplantation of animal-derived kidneys following targeted organ or blastocysts complementation. Some studies suggested that MSC are also able to differentiate into ectodermal and endodermal lineages, yet this pluripotent potential of MSC is still under debate. Because MSC extracted from bone marrow exhibit heterogeneous characteristics, phenotypic and functional equivalence is required for the use of MSC in any clinical context.
Based on these criteria, MSC have been isolated from a wide variety of fetal and adult tissues, including fetal amniotic fluid, placenta, umbilical cord, adipose tissue, endometrium, bone, kidney, lung, and liver. For therapies using human MSC hMSC , three distinct mechanisms can be discerned: 1 hMSC differentiate into a variety of cell types, which allow repair or reconstruction of bone tissue and cartilage; 21, 2 hMSC can modulate the microenvironment surrounding the injured tissue by secretion of immunosuppressive and anti-inflammatory factors that arrest cell cycle progression of invading immune cells, such as B cells, T cells, and macrophages.
Based on these secretive functions, hMSC are being explored as a cell-based therapy for myocardial injury, liver cirrhosis, and renovascular disease. In these models, bone marrow and adipose-derived MSC showed protective and regenerative effects via paracrine anti-inflammatory, anti-fibrotic, and vascularisation properties. Single infusion of hMSC 1.
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As the regenerative potential of hMSC for kidney disease remains controversial, more clinical evidence is needed to pinpoint the use of hMSC as a treatment for kidney disease. To establish an effective and stable hMSC-based therapy, several challenges are still looming. The function of hMSC is known to decline with age, as the culture expansion needed before hMSC transplantation is associated with cellular senescence.
Therefore, recommendations for the clinical use of hMSC are restricted to 3—5 passages. As such, nonclonal expansion of a heterogeneous population of hMSC is more likely to be adopted in a clinical setting, despite variations in efficacy. PSC are at the forefront of regenerative medicine in kidney disease by virtue of their unlimited self-renewal and capacity to differentiate into all types of renal cells, which provides possibilities to overcome the current shortage of donor kidneys.
Toyohara et al. On the contrary, Imberti et al. The results of these studies suggest that the transplantation site plays a crucial role in the therapeutic effect, rather than progenitor cell engraftment. To functionally restore or regenerate nephron structures within injured kidneys, engraftment of progenitor-like cells is indispensable. In the past decade, in-depth knowledge of mammalian kidney development has been translated into significant advances regarding directed differentiation of hiPSC into cells of the kidney lineage.
These so-called kidney organoids closely mimic the organisation of kidney epithelia, including structures expressing markers of podocytes, proximal tubules, loops of Henle, and distal tubules. Kidney organoids have been shown to facilitate the interrogation of renal toxicity, disease modelling, and mechanistic studies into human kidney development. In fact, NPC have been reported to form functional glomeruli and tubular structures in vivo. Table 1: Overview of studies exploring in vivo transplantation of renal progenitor cell, nephron progenitor cell, or nephron progenitor cell-derived tissues.
The study conducted by Sharmin et al. Although opt-out or presumed-consent strategies have been proposed as a way of increasing the supply of organs from deceased donors, they remain contentious. Acute kidney injury after a road-traffic collision may result from rhabdomyolysis and multi-organ failure as well as blunt or penetrating kidney injury.
Exposure to armed conflict can result in acute kidney injury caused by crush injury and rhabdomyolysis and the severity of injuries sustained in combat strongly correlates with the subsequent risk of chronic kidney disease. The net health burden of kidney disease is substantial, growing and driven by complex interactions, between communicable and noncommunicable diseases, that are shaped by upstream environmental and socioeconomic disparities.
Although kidney disease, whether acute, chronic or end-stage, can be extremely costly, it is also potentially preventable and adverse outcomes can often be delayed or prevented by inexpensive interventions. Kidney disease is highly prevalent, spans the life course and has substantial financial implications. Within each country, the local burden and prevalence of kidney disease and its risk factors and the local capacity to identify and manage such disease must be determined, as a prerequisite for fair priority setting and appropriate policy development.
Diagnosis of kidney disease is often hampered by a lack of awareness among health-care workers and at-risk communities and by inadequate and often erratic access to laboratory testing. Broad policies are increasingly being adopted globally to curb dietary intakes of fat, salt and sugar. Such policies all promise to reduce the burden of chronic kidney disease.
The burden of acute kidney injury could be reduced through the ongoing commitment to reduce the transmission of the pathogens causing infectious diseases. We need universal health coverage to tackle kidney disease successfully and ensure effective screening, prevention and early treatment. Effective and transparent policies to govern access to care for end-stage kidney disease should only be developed after there has been a thorough attempt to determine the local health priorities, especially in resource-poor settings. Engagement with all relevant stakeholders and innovative financing strategies will be required to maximize equitable access to care.
The bidirectional and synergistic interplay between kidney disease and all of the SGDs must be acknowledged in the development of a multisectoral approach. Monitoring the impact of policies on kidney disease and the risk factors for such disease needs to be integrated into existing surveillance activities. Health workers and communities must be empowered to advocate for, and hold policy-makers accountable for, kidney health, as an important step towards achievement of the SDGs.
Health Topics. World Health Statistics. About Us. Skip to main content. Bulletin of the World Health Organization. The 17 sustainable development goals and their relevance to kidney health, html, 10kb Global burden Although often considered a comorbidity of diabetes or hypertension, kidney disease has numerous complex causes.
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Table 2. Policy perspective The net health burden of kidney disease is substantial, growing and driven by complex interactions, between communicable and noncommunicable diseases, that are shaped by upstream environmental and socioeconomic disparities. Competing interests: None declared. Transforming our world: the agenda for sustainable development.
New York: United Nations; Global action plan for the prevention and control of noncommunicable diseases Geneva, Switzerland: World Health Organization; Geneva: World Health Organization; Global prevention and control of NCDs: limitations of the standard approach. J Public Health Policy. Global kidney health and beyond: a roadmap for closing gaps in care, research, and policy.
Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for causes of death, a systematic analysis for the Global Burden of Disease Study Worldwide access to treatment for end-stage kidney disease: a systematic review. Fact sheet [internet]. Global status report on noncommunicable diseases Global, regional, and national disability-adjusted life years DALYs for diseases and injuries and healthy life expectancy HALE for countries, quantifying the epidemiological transition.
Global, regional, and national age-sex specific mortality for causes of death, a systematic analysis for the Global Burden of Disease Study The contribution of chronic kidney disease to the global burden of major noncommunicable diseases. Kidney Int. Risk of coronary events in people with chronic kidney disease compared with those with diabetes: a population-level cohort study.