RCC blood vesselsinvade renal vein→if LEFT sided, may develop varicocele(精索静脈瘤)→IVC→hematogenous spread→metastasis to lung and bone urologyrenal HirotoShishido
when reabsorption ability of the nephron start to be saturated by the filtered load of glucosewhen serum glucose reaches 200〜375 mg/dL, glucose begins to appear in urine renal HirotoShishido
輸入細動脈、輸出細動脈、緻密班、傍糸球体細胞afferent arteriole,efferent arteriole,macula densa,jaxtaglomerular(JG) cells medical termrenal HirotoShishido
which chromosomal aneuploidy syndromes are associated w/ horseshoe kidneyturner syndrome, trisomies 13,18,21 renalurology HirotoShishido
the reason why NSAIDs cause the harmful effect to the patients with volume depletionIn the patient who have volume depletion such as heart failure, there is increased secretion of the vasoconstrictors angiotensin Ⅱ, norepinephrine. In these cases,there is increased secretion of prostagrandins to maintain renal blood flow by counteracting the vasoconstrictive effects. When prostagrandin synthesis is inhibited, preglomerular resistance increases, and renal blood flow is reduced leading to acute renal failure. renal HirotoShishido
Renal segment which is damaged first and severely¥straight segment of proximal tubule (PST) and the distal straight tubule (aka thick ascending limb, or TAL) are both located in the outer renal medulla and are the nephron segments damaged first and most severely during renal hypoperfusion. renalAmboss level4 HirotoShishido
fanconi syndrome
manifestationpolyuria, polydipsia, and ☆failure to thrive tend to occur in the first years of life
☆Glucose, bicarbonate, amino acids, calcium, and phosphate are normally filtered by the glomerulus and reabsorbed by the proximal tubule. When proximal tubular transport is defective (as in Fanconi syndrome), these substances appear in the urine despite being present at normal concentrations in serum. renalUWorld HirotoShishido
drug induced fanconi syndromecytoplasmic vacuolization and intracytoplasmic inclusions in the PCT
