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renal pathology associated with sclerosis of renal arterioles and small arteries, resultant effect - focal ischemia of parenchyma supplied by vessels with thickened walls and consequent narrowed lumen what is the loss of mass from benign nephrosclerosis due to? What are some of the other changes? form of renal disease associated with malignant or accelerated phase of hypertension what do patients with malignant hypertension have? consequences of markedly elevated blood pressure on blood vessels throughout body what is the the morphology of malignant nephrosclerosis fibrionoid necrosis of arterioles gives what type of appearance in malignant nephrosclerosis? due to stimulation of renin secretion by cells of the juxtaglomerular apparatus, and subsequent production of the vasoconstrictor angiotensin II - large proportion of individuals with renovascular hypertension have elevated plasma or renal vein renin levels and almost all show a reduction of blood pressure when given drugs that block activity of angiotensin II most common cause of renal artery stenosis is, occurs frequently in men, 2nd type of lesion leading to stenosis is group of disorders is characterized by microangiopathic hemolytic anemia, thrombocytopenia, and in many causes renal failure, and morphologically by thrombotic lesions in capillaries and arterioles in various tissue beds, including those of the kidney most frequently associated with consumption of food contaminated by bacteria producing Shiga-like toxins occurs following intestinal infection with strains of E.coli - sudden onset of bleeding manifestations, severe oliguria and hematuria, associated with microangiopathic hemolytic anemia 1. inherited mtuations of complement-regulatory proteins 2. diverse acquired causes of endothelial injury, including antiphospholipid antibodies, complications of pregnancy and oral contraceptives, vascular renal diseases, chemotherapeutic and immunosuppressive drugs, radiation - most commonly affects factor H, which normally breaks down alternative pathway C3 convertase and protects cells from damage by uncontrolled complement activation often associated with inherited or acquired deficiencies of ADAMTS13, a plasma metalloprotease that regulates function of von Willebrand factor (vWF) benign nephrosclerosis
cortical scarring and shrinking; patchy ischemic atrophy, consists of 1. foci of tubular atrophy and interstitial fibrosis 2. variety of glomerular alterations malignant hypertension and accelerated nephrosclerosis markedly elevated levels of plasma renin malignant arteriosclerosis small, pinpoint petechial hemorrhages may appear on the cortical surface from rupture of arterioles or glomerular capillaries, gives kidney 'flea-bitten' appearance onion-skinning because of its concentric appearance renal artery stenosis
occlusion by an atheromatous plaque at the origin of the renal artery; fibromuscular dysplasia thrombotic microangiopathies
TTP
sickle cell disease nephropathy; hematuria and diminished concentrating ability, patchy papillary necrosis, proteinuria common diffuse cortical necrosis - has features of ischemic necrosis renal infarcts clinically silent, but sometimes pain and tenderness localized to the costovertebral angle, associated with shower of red cells in urine Agenesis of the kidney Renal hypoplasia Multicystic renal dysplasia
Multicystic renal dysplasia ADPKD Nephrons, so renal function is retained until the 4 th or 5th decade PKD1 Cellular proliferation, basal levels of apoptosis, interactions with the ECM, and secretory function of the epithelia
Morphology of autosomal-recessive (childhood) polycystic kidney disease Patients who survive infancy and juvenile usually have Lesions consisting of multiple cystic dilations of the collecting ducts in the medulla, adults, Presence of a variable number of cysts in the medulla, usually concentrated at the corticomedullary junction; cortical tubulointerstitial damage is the cause of eventual renal insufficiency Affected children present first with polyuria and polydipsia, sodium wasting and tubular acidosis also prominent Cysts contain clear fluid, lined by either hyperplastic or flattened tubular epithelium, can develop into renal cell carcinoma Causes of urinary tract obstruction
Describes dilation of the renal pelvis and calyces associated with progressive atrophy of the kidney due to obstruction to the outflow of urine Morphology of UTO
Earliest manifestation is inability to concentrate the urine reflected by polyuria and nocturia, distal tubular acidosis, renal salt wasting, secondary renal calculi, and chronic tubulointerstitial nephritis with scarring and atrophy of the papilla and medulla Results in oliguria or anuria Four main types of calculi
When obstruction is sudden and complete, GFR is reduced, there is dilation of the pelvis and calyces, and often significant interstitial inflammation Bilateral partial obstruction
Type of stone formed largely after bacterial infections Type of stone common in individuals with hyperuricemia and diseases involving high cell turnover
Complete bilateral obstruction 1. Calcium stones- composed of calcium oxalate 2. Triple stones/struvite stones- composed of magnesium ammonium phosphate 3. Uric acid stones 4. Cysteine stones Magnesium ammonium phosphate Uric acid stone
Angiomyolipoma Oncocytoma
Renal cell carcinoma Von hippel-lindau syndrome, hereditary clear cell carcinoma, hereditary papillary carcinoma Clear cell carcinoma Papillary carcinoma
Renal cell carcinomas also produce a number of One of the most common characteristics of RCC Most common locations of metastases for RCC Produce noticeable hematuria, may block urinary outflow and lead to palpable hydronephrosis and flank pain. Prognosis for this tumor is not good
CV pain, palpable mass, and hematuria (also associated with generalized constitutional symptoms such as fever, malaise, weakness and weight loss) Paraneoplastic syndromes Tendancy to give rise to metastases before giving rise to local signs or symptoms Lungs and bones Urothelial carcinomas of the renal pelvis