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Minarcik robbins 2013_ch20-kidney
 

Minarcik robbins 2013_ch20-kidney

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  • The human kidney is a product of the metanephric system. <br /> Recall, pronephros, mesonephros, metanephros, woolffian, muellerian. <br />
  • Sallow = 196, 145, 141 (RGB) <br />
  • Salix caprea <br />
  • Mutations in EYA1 or SIX1 genes have been associated with multicystic renal dysplasia. <br />
  • How many kidneys in your cadaver lab had NO cysts whatsoever? Probably not many? <br />
  • Even though there are MANY types of glomerulonephropathies, here are some of the common findings seen in many of them. <br />
  • Here is the warzone of the glomerulopathies: 1) podocytes, 2) basement membrane, 3) endothelium <br />
  • Why is the pic on the left classic for glomerulonephritis? Ans: Inflammatory cell infiltrates in the glomeruli <br />
  • Recent studies have suggested that crescents are primarily of monocytic origin. They are signs that ANY glomerulonephritis may be severe or “rapidly progressing”, i.e., death within 3 months usually. <br />
  • To make a long story short, the NEPHROTIC SYMDROME is usually a sign of a glomerulonephropathy. <br />
  • What does indolent mean? <br /> “Causing little or no pain; inactive or relatively benign” <br />
  • The ability to recognize the BM as being rather uniform in thickness and density is so critically important <br />
  • Once again, as in “chronic” pancreatitis, the main features of “chronic” are more a fibrosis (hyalinization), rather than lymph and macrophage infiltrates. <br />
  • What percentage of these tubules are PROXIMAL convoluted tubules rather than DISTAL? Answer: 98% <br />
  • The “necrotic” tubular cells are karryolytic. <br />
  • Pitting geographic “scars” is the hallmark of chronic pyelonephritis. <br />
  • “THYROIDIZATION” is another common hallmark of chronic pyelonephritis. <br /> To my knowledge, this is one of 3 things which look like thyroid, but are not. What are the other two? 1) Pars intermedia of pituitary 2) lactation breast lobule <br />
  • What are the 3 parts of the ureter which are most subject to obstruction or stones for anatomic reasons alone? <br /> UPJ, pelvic brim, bladder inlet <br />
  • Is the primary inflammatory focus in the tubules or interstitium BETWEEN the tubules? <br />
  • What is “metastatic” calcification? Ans: The tissue calcification due to hypercalcemia <br />
  • Differentiate Bence-Jones protein from amyloid <br />
  • Is it fair to say just about all of the primary vascular diseases of the kidney might result in hypertension” Answer: YES <br />
  • Does the name “malignant” imply, perhaps, EXTREME blood pressure elevations? Answer: YES <br />
  • Could fibrin plugs in small vessels easily be missed if a fibrin stain is not done, thinking this is merely blood? Answer: YES <br />
  • Is the CORTEX of a kidney MUCH more susceptible than a MEDULLA to ischemia? Answer: YES <br />
  • What is an “anemic” infarct? Ans: It is an infarct which is grossly pale in the acute stage because of lack of collateral circulation. <br />
  • The principle of ANY bodily tubular obstruction is that the part UPSTREAM from the obstruction may have increased pressure or become, therefore, dilated. <br /> The part DOWN stream from the obstruction does not get fed and therefore can become atrophic, necrotic, or inflamed. <br /> This is a CLASSICAL powerpoint slide where you are, once again, being asked to THINK like a pathologist! <br />
  • What is a “staghorn” calculus? <br />
  • Which tumor is “papillary”, which tumor has “oncocytes”, which tumor has fat and vessels, which tumor has spindly fibroblasts and collagen? Could you match these 4 pics up with these 4 benign tumors? Papillary Adenoma, Fibroma/Hamartoma, Angiomyolipoma, Oncocytoma <br /> Why are oncocytes very RED and granular? <br />
  • Hematuria and pain are the two commonest symptoms, but there are NO consistent reliable early symptoms usually. <br /> Would a urothelial (transitional pelvic) carcinoma be more likely to produce hematuria early than a clear cell? Ans: YES <br />
  • Angiogram, CT, Gross, Microscopic, respectively. Show the tumor in each one. Clear cell carcinoma nuclei classically look “benign”, i.e., small, uniform, centrally located. <br /> What does YELLOW on gross and CLEAR on micro mean? Answer: FAT <br />
  • The most likely place for a transitional (urothelial) carcinoma, is smack dab in the HILUM! (because that’s where the transitional mucosa is) <br />

Minarcik robbins 2013_ch20-kidney Minarcik robbins 2013_ch20-kidney Presentation Transcript

  • KIDNEY
  • RENAL PATHOLOGY • NORMAL • CONGENITAL • “CYSTS” • GLOMERULAR • TUBULAR/INTERSTITIAL • BLOOD VESSELS • OBSTRUCTION • TUMORS
  • 1. Renal Vein 2. Renal Artery 3. Renal Calyx 4. Medullary Pyramid 5. Renal Cortex 6. Segmental Artery 7. InterlobAR Artery 8. Arcuate Artery interlobULAR 9. Arcuate Vein 10. Interlobar Vein 11. Segmental Vein 12. Renal Column 13. Renal Papillae 14. Renal Pelvis 15. Ureter
  • S.E.M. T.E.M.
  • CHRONIC RENAL FAILURE Fluid and Electrolytes: Dehydration, Edema, Hyperkalemia, Metabolic acidosis Calcium Phosphate and Bone: Hyperphosphatemia, Hypocalcemia, Secondary hyperparathyroidism, Renal osteodystrophy Hematologic: Anemia, Bleeding diathesis Cardiopulmonary: Hypertension, Congestive heart failure, Pulmonary edema, Uremic pericarditis Gastrointestinal: Nausea and vomiting, Bleeding, Esophagitis, gastritis, colitis Neuromuscular: Myopathy, Peripheral neuropathy, Encephalopathy Dermatologic: Sallow (greenish-yellow) color, Pruritus, Dermatitis
  • CONGENITAL • AGENESIS • HYPOPLASIA • ECTOPIC • HORSESHOE
  • AGENESIS
  • HYPOPLASIA
  • ECTOPIC (usually PELVIC)
  • HORSESHOE
  • CYSTIC DISEASES • CYSTIC RENAL “DYSPLASIA” • Autosomal DOMINANT (AD-ULTS) • Autosomal RECESSIVE (CHILDREN) • MEDULLARY – Medullary Sponge Kidney (MSK) – Nephronopththisis-Medullary • ACQUIRED • SIMPLE
  • CYSTIC RENAL “DYSPLASIA” • • • • • • ENLARGED UNILATERAL or BILATERAL CYSTIC Have “MESENCHYME” NEWBORNS VIRAL, GENETIC (rare)
  • AUTOSOMAL DOMINANT • HEREDITARY, PKD1, PKD2 • FOLLOWS AUTOSOMAL DOMINANT PEDIGREE • COMPLEX GENETICS • RENAL FAILURE in 50’s
  • AUTOSOMAL RECESSIVE • CHILDHOOD • KIDNEYS LOOK EXACTLY LIKE THE ADULT TYPE • PKHD1 • PATIENTS WHO SURVIVE CHILDHOOD OFTEN DEVELOP HEPATIC FIBROSIS
  • MEDULLARY CYSTS • MEDULLARY SPONGE KIDNEY (MSK), usually an incidental finding on CT or US • NEPHRONOPHTHISIS, cysts @ CMJ, hereditary (AR), progressive
  • ACQUIRED (DIALYSIS)
  • “SIMPLE” CYSTS • Cortical • Also called “retention” cysts • Also “acquired” • Incidental, asymptomatic • VERY very very common
  • GLOMERULAR DISEASES aka, glomerulonephropathies
  • CLINICAL MANIFESTATIONS • ACUTE NEPHROTIC SYNDROME • RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS • NEPHROTIC SYNDROME • CHRONIC RENAL FAILURE • ASYMPTOMATIC HEMATURIA or PROTEINURIA
  • PATHOLOGIC MANIFESTATIONS • CELLULAR PROLIFERATION – Mesangial – Endothelial • • • • • LEUKOCYTE INFILTRATION CRESCENTS (RAPIDLY progressive) BASEMENT MEMBRANE THICKENING HYALINIZATION SCLEROSIS
  • PATHOGENESIS • • • • Antibodies against inherent GBM Antibodies against “planted” antigens Trapping of Ag-Ab complexes Antibodies against glomerular cells, e.g., mesangial cells, podocytes, etc. • Cell mediated immunity, i.e., sensitized Tcells as in TB
  • MEDIATORS • NEUTROPHILS, MONOCYTES • MACROPHAGES, T-CELLS, NK CELLS • PLATELETS • MESANGIAL CELLS • SOLUBLE: CYTOKINES, CHEMOKINES, COAGULATION FACTORS
  • ACUTE GLOMERULONEPHRITIS • Hematuria, Azotemia, Oliguria, in children following a strep infection • POSTSTREPTOCOCCAL (old term) • HYPERCELLULAR GLOMERULI • INCREASED ENDOTHELIUM AND MESANGIUM • IgG, IgM, (not IgA), C3 along GMB FOCALLY • 95% full recovery
  • “RAPIDLY PROGRESSIVE” GLOMERULONEPHRITIS • Clinical definition, NOT a specific pathologic one • “CRESCENTIC” • Anti-GBM Ab • IMMUN CPLX • Anti-Neut. Ab
  • NEPHROTIC SYNDROME • MASSIVE PROTEINURIA • HYPOALBUMINEMIA • EDEMA • LIPIDEMIA/LIPIDURIA • NUMEROUS CAUSES: – MEMBRANOUS, MINIMAL CHANGE, FOCAL SEGMTL. – DIABETES, AMYLOID, SLE, DRUGS
  • MEMBRANOUS GLOMERULONEPHRITIS • • • • Drugs, Tumors, SLE, Infections Deposition of Ag-Ab complexes Indolent, but >60% persistent proteinuria 15% go on to nephrotic syndrome
  • MINIMAL CHANGE GLOM. (LIPOID NEPHROSIS) • MOST COMMON CAUSE of NEPHROTIC SYNDROME in CHILDREN • EFFACEMENT of FOOT PROCESSES
  • FOCAL SEGMENTAL GLOMERULO-SCLEROSIS • Just like its name – Focal – Segmental – Glomerulo-SCLEROSIS (NOT –itis) • HIV, Heroine, Sickle Cell, Obesity • Most common cause of ADULT nephrotic syndrome
  • MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS • MPGN can be idiopathic or 2º to chronic immune diseases Hep-C, alpha-1antitrypsin, HIV, Malignancies • GBM alterations, subendo. • Leukocyte infiltrations • Predominant MESANGIAL involvement
  • IgA NEPHROPATHY (BERGER DISEASE) • Mild hematuria • Mild proteinuria • IgA deposits in mesangium
  • HEREDITARY HEMATURIA SYNDROMES • ALPORT SYNDROME – Progressive Renal Failure – Nerve Deafness – VARIOUS eye disorder – DEFECTIVE COLLAGEN TYPE IV • THIN GBM (Glomerular Basement Membrane) Disease, i.e., about HALF as uniformly thin as it should be
  • CHRONIC GLOMERULONEPHRITIS • Can result from just about ANY of the previously described acute ones – THIN CORTEX – HYALINIZED (fibrotic) GLOMERULI – OFTEN SEEN IN DIALYSIS PATIENTS
  • SECONDARY (2º) GLUMERULONEPHROPATHIES • • • • • • • • SLE Henoch-Schonlein Purpura (IgA-NEPH) BACTERIAL ENDOCARDITIS DIABETES (Nodular Glomerulosclerosis, or K-W Kidney) AMYLOIDOSIS GOODPASTURE WEGENER MYELOMA
  • TUBULES INTERSTITIUM BLOOD VESSELS OBSTRUCTION TUMORS
  • TUBULAR DISEASES • ACUTE TUBULAR NECROSIS • TUBULOINTERSTITIAL NEPHRITIS – PYELONEPHRITIS • ACUTE • CHRONIC – DRUGS – TOXINS • URATE NEPHROPATHY • HYPERCALCEMIA/NEPHROCALCINOSIS • MULTIPLE MYELOMA
  • ACUTE TUBULAR NECROSIS • • • • Destruction of renal TUBULAR epithelium Loss of renal function 50% of ACUTE renal failure Two types: ISCHEMIC NEPHROTOXIC -AMINOGLYCOSIDES -AMPHOTERICIN B -CONTRAST AGENTS
  • NORMAL
  • ATN
  • ATN PATHOGENESIS • BLOOD FLOW DISTURBANCES (ISCHEMIC) • TUBULAR INJURY (NEPHROTOXIC)
  • CLINICAL COURSE • INITIATION (36 hours) – Mild OLIGURIA – Mild AZOTEMIA • MAINTENANCE – More OLIGURIA – More AZOTEMIA – DIALYSIS NEEDED • RECOVERY – HYPOKALEMIA main problem – BUN, CREATININE return to normal
  • TUBULO/INTERSTITIAL NEPHRITIS • INFECTIONS, i.e., pyelonephritis • TOXINS, heavy metals, chemo, NSAIDS • METABOLIC, urates, Ca++, Oxalates • PHYSICAL, obstruction, radiation • IMMUNOLOGIC, esp. transplant rejection
  • PYELONEPHRITIS • GI Gram NEGATIVES: E. COLI, Proteus, Klebsiella, Enterobacter, Strep. faecalis, usually “NORMAL” flora • ASCENDING, by FAR, the most common, i.e., reflux, obstruction • HEMATOGENOUS too • ACUTE PYELONEPHRITIS, neutrophils • CHRONIC PYELONEPHRITIS, lymphocytes, scars
  • ACUTE or CHRONIC PYELONEPHRITIS?
  • ACUTE or CHRONIC PYELONEPHRITIS?
  • ACUTE or CHRONIC PYELONEPHRITIS?
  • • • • • • • • FACTORS OBSTRUCTION: Congenital or Acquired INSTRUMENTATION VESICOURETERAL REFLUX PREGNANCY AGE, SEX, why sex? F>>>M PREVIOUS LESIONS IMMUNOSUPPRESION or IMMUNODEFICIENCY
  • DRUGS/TOXINS causing INTERSTITIAL NEPHRITIS • Synthetic Penicillins • Rifampin • Thiazides • 2 weeks later: Fever, eosinophilia, rash, and an acute renal failure type of picture
  • ANALGESIC NEPHROPATHY • ASPIRIN, TYLENOL, NSAIDS – TUBULOINTERSTITIAL NEPHRITIS – PAPILLARY NECROSIS (also Dm & HbS)
  • URATE NEPHROPATHY • Precipitation of Uric Acid Crystals in the TUBULES, especially in a LOWER than usual PH situation (mini-TOPHUS) H & E alcohol fixed POLARIZED LIGHT MICROSCOPY
  • HYPERCALCEMIA NEPHROCALCINOSIS PRINCIPLE: In extreme or uncontrolled or chronic HYPERCALCEMIA, calcium stones form in the tubulo-interstitium of the kidney, which can eventually lead to tubular obstruction and loss of function
  • MULTIPLE MYELOMA • Bence Jones proteinuria (immunoglobulin light chains) • AMYLOIDOSIS
  • NORMAL
  • VASCULAR DISEASES • BENIGN NEPHROSCLEROSIS • MALIGNANT NEPHROSCLEROSIS (i.e., malignant hypertension) • RENAL ARTERY STENOSIS • THROMBOTIC MICROANGIOPATHIES – Hemolytic-Uremic Syndromes, Child, Adult, TTP • THROMBI, EMBOLI, INFARCTS – SICKLE CELL – DIFFUSE CORTICAL NECROSIS
  • BENIGN NEPHROSCLEROSIS • Sclerosis, i.e., “hyalinization” of arterioles and small arteries, i.e., arterio-, arteriolo• Is this part of “routine” atherosclerosis???? • VERY VERY VERY common
  • MALIGNANT NEPHROSCLEROSIS (i.e., malignant hypertension) • NOT a part of “routine” atherosclerosis • By definition, associated with rapidly progressive hypertension (1-2% of HTN) • VASCULAR DAMAGE • FIBRINOID NECROSIS • “ONION SKINNING” • SIGNIFICANT LUMENAL NARROWING
  • What is “onion-skinning”? What is an onion? What is “fibrinoid” necrosis?
  • Renal Artery Stenosis • Rare cause of HTN • SMALL Kidney • 1) Plaque type is usual cause, yes regular old atherosclerosis • 2) Fibromuscular “dysplasia” type: – INTIMAL HYPERPLASIA – MEDIAL HYPERPLASIA – ADVENTITIAL HYPERPLASIA – In younger women
  • PLAQUE, i.e., FIBROMUSCULAR ATHEROSCLEROSIS DYSPLASIA
  • MICROANGIOPATHIES (thrombotic) • Hemolytic-Uremic Syndrome – Familial – Childhood – Adult • TTP (Thrombotic Thrombocytopenic Purpura), IDIOPATHIC
  • MICROANGIOPATHIES COMMON PROCESSES – Hemolysis – Thromboses in renal capillaries – Thrombocytopenia (a “consumption” coagulopathy) – FIBRIN PLUGS
  • OTHER VASCULAR • • • • Atherosclerosis Atheroemboli Sickle Cell Diffuse Cortical Necrosis
  • RENAL INFARCTS • WEDGE SHAPED • WELL DELINEATED • “WHITE” (anemic) INFARCT • Perhaps a little “YELLOW” • HEAL WITH A SCAR
  • OBSTRUCTIONS • UROLITHIASIS • • • • • • • CONGENITAL PROSTATE ENLARGEMENT TUMORS INFLAMMATION SLOUGHED CLOTS, PAPILLAE PREGNANCY NEUROGENIC
  • UROLITHIASIS • CALCIUM (OXALATE or PHOSPHATE) 70% CA↑↑↑ • MAGNESIUM AMMONIUM PHOSPHATE • URIC ACID 20% 10% Bact. U.A. ↑↑↑
  • TUMORS • BENIGN – Papillary Adenoma (SIZE very important) – Fibroma/Hamartoma – Angiomyolipoma – Oncocytoma (very red, granular, mitochondria) • MALIGNANT – Renal Cell Carcinoma (Clear Cell Carcinoma, Adenocarcinoma, Hypernephroma) – Urothelial (Transitional)
  • RENAL CELL CARCINOMA • TOBACCO RELATED, STRONGLY • SOME HEREDITARY/FAMILIAL • MOST are “CLEAR CELL”, a few PAPILLARY • YELLOW grossly, “CLEAR” cells microscopically • STRONGLY tend to invade the renal VEIN early, in preference to lymphatics. Does the kidney have lymphatics?
  • UROTHELIAL (TRANSITIONAL) RENAL CARCINOMAS • In renal pelvis. Why? • 1/10 as common as renal cell carcinomas • EXACTLY the same appearance as lower urinary tract carcinomas. Why? • MUCH more likely to obstruct and cause hematuria early than renal (clear) cell carcinomas. Why? • Associated with ureter and bladder carcinomas. Why?