Ebook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2
➤ Gửi thông báo lỗi ⚠️ Báo cáo tài liệu vi phạmNội dung chi tiết: Ebook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2
Ebook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2
SECTION IVGLOMERULARAND TUBULARDISORDERSTwo human kidneys harbor nearly 1.8 million glomerular capillar)' tufts. Each glomerular tuft resides within B Ebook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2Bowman's space. The capsule circumscribing this space is lined by parietal epithelial cells that transition into tubular epithelia forming the proximal nephron or migrate into the tuft to replenish podocytes. The glomerular capillary tuft derives from an afferent arteriole that forms a branching cap Ebook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2illary bed embedded in mesangial matrix (Fig. 15-1). This capillary' network funnels into an efferent arteriole, which passes filtered blood into cortEbook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2
ical peritubular capillaries or medullary' vasa recta that supply and exchange with a folded tubular architecture. Hence the glomerular capillary' tufSECTION IVGLOMERULARAND TUBULARDISORDERSTwo human kidneys harbor nearly 1.8 million glomerular capillar)' tufts. Each glomerular tuft resides within B Ebook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2) line glomerular capillaries. Delicate foot processes extending from epithelial podocytes shroud the outer surface of these capillaries, and podocytes interconnect to each other by slit-pore membranes forming a selective filtration barrier.The glomerular capillaries filter 120-180 L/d of plasma wat Ebook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2er containing various solutes for reclamation or discharge by downstream tubules. Most large proteins and all cells are excluded from filtration by aEbook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2
physicochemical barrier governed by pore size and negative electrostatic charge. The mechanics of filtration and reclamation are quite complicated forSECTION IVGLOMERULARAND TUBULARDISORDERSTwo human kidneys harbor nearly 1.8 million glomerular capillar)' tufts. Each glomerular tuft resides within B Ebook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2tend to repel the negatively charged GBM, it only has a physical radius of 3.6 nm, while pores in the GBM and slit-pore membranes have a radius of 4 nm. Consequently, variable amounts of albumin inevitably cross the filtration barrier to be reclaimed by megalin and cubilin receptors along the proxim Ebook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2al tubule. Remarkably, humans with normal nephrons do not excrete more than 8-10 mg of albumin in daily voided urine, approximately 20-60% of total exEbook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2
creted protein. This amount of albumin, andother proteins, can rise to gram quantities following glomerular injury.The breadth of diseases affecting tSECTION IVGLOMERULARAND TUBULARDISORDERSTwo human kidneys harbor nearly 1.8 million glomerular capillar)' tufts. Each glomerular tuft resides within B Ebook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2 changes to urinalysis. Some order to this vast subject is brought by grouping all of these diseases into a smaller number of clinical syndromes.PATHOGENESIS OF GLOMERULAR DISEASEThere are many forms of glomerular disease with pathogenesis variably linked to the presence of genetic mutations, infect Ebook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2ion, toxin exposure, autoimmunity, atherosclerosis, hypertension, emboli, thrombosis, or diabetes mel-litus. Even after careful study, however, the caEbook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2
use often remains unknown, and the lesion is called idiopathic. Specific or unique features of pathogenesis are mentioned with the description of eachSECTION IVGLOMERULARAND TUBULARDISORDERSTwo human kidneys harbor nearly 1.8 million glomerular capillar)' tufts. Each glomerular tuft resides within B Ebook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2t: congenital nephrotic syndrome from mutations in NPHSÍ (nephrm) and NI*HS2 (podocin) affect the slit-pore membrane at birth, and TRPC6 cation channel mutations produce focal segmental glomerulosclerosis (FSCS) in adulthood; polymorphisms in the gene encoding apolipoprotein LI (APOL1) are a major r Ebook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2isk for nearly 70% of African Americans with nondiabetic end-stage renal disease (ESRD), particularly FSGS; mutations in complement factor H associateEbook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2
d with mcmbranoprolifera-tive glomerulonephritis (MPGN) or atypical hemolytic uremic syndrome (aHUS), type II partial lipodystrophy from mutations in SECTION IVGLOMERULARAND TUBULARDISORDERSTwo human kidneys harbor nearly 1.8 million glomerular capillar)' tufts. Each glomerular tuft resides within B Ebook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2ic factor; Alport's syndrome, from mutations162163DBowman's capsulePodocyteBowman's spaceParietal epitheliaCapillary stalkGlomerular capillary endotheliaMesangiumGlomerular basement membraneFIGURE 15-1Glomerular architecture. A. The glomerular capillaries form from a branching network of renal arter Ebook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2ies (arterioles) lead-ing to an afferent arteriole, glomerular capillary bed (tuft), and a draining efferent arteriole. (From VH Gattone II et al: HypEbook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2
ertension 5:8. 1983.} B. Scanning electron micrograph of podocytes that line the outer surface of the glomerularcapillaries (arrow shows foot process)SECTION IVGLOMERULARAND TUBULARDISORDERSTwo human kidneys harbor nearly 1.8 million glomerular capillar)' tufts. Each glomerular tuft resides within B Ebook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2ght microscopy. (A-C. courtesy of Dr. Vincent Gattone. Indiana University: with permission.}in the genes encoding for the Ct3. (Z4, or Ừ.5 chains of type IV collagen, produces split-basement membranes with glomerulosclerosis', and lysosomal storage diseases, such as ơ-galactosidase A deficiency caus Ebook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2ing Fabry's disease and N-acetylneuraminic acid hydrolase deficiency causing nephrosialidosis, produce FSGS.Systemic hypertension and atherosclerosisEbook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2
can produce pressure stress, ischemia, or lipid oxidants that lead to (hronic glomerulosclerosis. Malignant hypertension can quickly complicate glomerSECTION IVGLOMERULARAND TUBULARDISORDERSTwo human kidneys harbor nearly 1.8 million glomerular capillar)' tufts. Each glomerular tuft resides within B Ebook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2ired sclerotic injury associated with thickening of the GBM secondary' to the long-standing effects of hyperglycemia, advanced glycosylation end products, and reactive oxygen species.Inflammation of the glomerular capillaries is called glomerulonephritis. Most glomerular or mesangial antigens involv Ebook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2ed in immune-mediated glomerulonephritis areunknown (Fig. 15-2). Glomerular epithelial or mesangial cells may shed or express epitopes that mimic otheEbook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2
r immunogenic proteins made elsewhere in the body. Bacteria, fiingi, and viruses can directly infect the kidney producing their own antigens. AutoimmuSECTION IVGLOMERULARAND TUBULARDISORDERSTwo human kidneys harbor nearly 1.8 million glomerular capillar)' tufts. Each glomerular tuft resides within B Ebook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2ephritis or granulomatosis with polyangiitis (Wegener’s) spread to the kidney, causing secondary glomerular injury. Anfiglomerular basement membrane disease producing Goodpasture's syndrome primarily injures both the lung and kidney because of the narrow distribution of the a? NCI domain of type IV Ebook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2collagen that is the target antigen.Local activation of toll-like receptors on glomerular cells, deposition of immune complexes, or complement injuryEbook Harrison''s nephrology and acid-base disorders (2nd edition): Part 2
to glomerular structures induces mononuclear cell infiltration, which subsequently leads to an adaptive immune response attracted to the kidney by locSECTION IVGLOMERULARAND TUBULARDISORDERSTwo human kidneys harbor nearly 1.8 million glomerular capillar)' tufts. Each glomerular tuft resides within BSECTION IVGLOMERULARAND TUBULARDISORDERSTwo human kidneys harbor nearly 1.8 million glomerular capillar)' tufts. Each glomerular tuft resides within BGọi ngay
Chat zalo
Facebook