1. RENAL PATHOLOGY GLOMERULAR TUBULAR/INTERSTITIAL BLOOD VESSELS NORMAL
CONGENITAL
“CYSTS”
GLOMERULAR
TUBULAR/INTERSTITIAL
BLOOD VESSELS
OBSTRUCTION
TUMORS

3. 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

5. T.E.M.
S.E.M.

7. CONGENITAL
AGENESIS
HYPOPLASIA
ECTOPIC
HORSESHOE

8. AGENESIS

9. HYPOPLASIA

10. ECTOPIC (usually PELVIC)

11. HORSESHOE

12. CYSTIC DISEASES Autosomal DOMINANT (AD-ULTS) CYSTIC RENAL “DYSPLASIA”
Autosomal RECESSIVE (CHILDREN)
MEDULLARY
Medullary Sponge Kidney (MSK)
Nephronopththisis-Medullary
ACQUIRED
SIMPLE

13. CYSTIC RENAL “DYSPLASIA”
ENLARGED
UNILATERAL or BILATERAL
CYSTIC
Have “MESENCHYME”
NEWBORNS
VIRAL, GENETIC (rare)
Mutations in EYA1 or SIX1 genes have been associated with multicystic renal dysplasia.

14. AUTOSOMAL DOMINANT HEREDITARY, PKD1, PKD2
FOLLOWS AUTOSOMAL DOMINANT PEDIGREE
COMPLEX GENETICS
RENAL FAILURE in 50’s

15. AUTOSOMAL RECESSIVE CHILDHOOD KIDNEYS LOOK EXACTLY LIKE THE ADULT TYPE
PKHD1
PATIENTS WHO SURVIVE CHILDHOOD OFTEN DEVELOP HEPATIC FIBROSIS

16. ACQUIRED (DIALYSIS)

17. “SIMPLE” CYSTS Cortical Also called “retention” cysts Also “acquired”
Incidental, asymptomatic
VERY very very common
How many kidneys in your cadaver lab had NO cysts whatsoever? Probably not many?

19. GLOMERULAR DISEASES aka, glomerulonephropathies

20. PATHOLOGIC MANIFESTATIONS
CELLULAR PROLIFERATION
Mesangial
Endothelial
LEUKOCYTE INFILTRATION
CRESCENTS (RAPIDLY progressive)
BASEMENT MEMBRANE THICKENING
HYALINIZATION
SCLEROSIS
Even though there are MANY types of glomerulonephropathies, here are some of the common findings seen in many of them.

21. 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 T-cells as in TB

22. Here is the warzone of the glomerulopathies: 1) podocytes, 2) basement membrane, 3) endothelium

23. 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

24. Why is the pic on the left classic for glomerulonephritis
Why is the pic on the left classic for glomerulonephritis? Ans: Inflammatory cell infiltrates in the glomeruli

25. “RAPIDLY PROGRESSIVE” GLOMERULONEPHRITIS
Clinical definition, NOT a specific pathologic one
“CRESCENTIC”
Anti-GBM Ab
IMMUN CPLX
Anti-Neut. Ab
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.

26. NEPHROTIC SYNDROME MASSIVE PROTEINURIA HYPOALBUMINEMIA EDEMA
LIPIDEMIA/LIPIDURIA
NUMEROUS CAUSES:
MEMBRANOUS, MINIMAL CHANGE, FOCAL SEGMTL.
DIABETES, AMYLOID, SLE, DRUGS
To make a long story short, the NEPHROTIC SYMDROME is usually a sign of a glomerulonephropathy.

27. MEMBRANOUS GLOMERULONEPHRITIS
Drugs, Tumors, SLE, Infections
Deposition of Ag-Ab complexes
Indolent, but >60% persistent proteinuria
15% go on to nephrotic syndrome
What does indolent mean?
“Causing little or no pain; inactive or relatively benign”

29. MINIMAL CHANGE GLOM. (LIPOID NEPHROSIS)
MOST COMMON CAUSE of NEPHROTIC SYNDROME in CHILDREN
EFFACEMENT of FOOT PROCESSES
The ability to recognize the BM as being rather uniform in thickness and density is so critically important

30. 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

32. TUBULES INTERSTITIUM BLOOD VESSELS OBSTRUCTION TUMORS

33. TUBULAR DISEASES ACUTE TUBULAR NECROSIS TUBULOINTERSTITIAL NEPHRITIS
PYELONEPHRITIS
ACUTE
CHRONIC
DRUGS
TOXINS
URATE NEPHROPATHY
HYPERCALCEMIA/NEPHROCALCINOSIS
MULTIPLE MYELOMA

34. 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

35. NORMAL
What percentage of these tubules are PROXIMAL convoluted tubules rather than DISTAL? Answer: 98%

36. ATN
The “necrotic” tubular cells are karryolytic.

37. ATN PATHOGENESIS BLOOD FLOW DISTURBANCES (ISCHEMIC)
TUBULAR INJURY (NEPHROTOXIC)

38. 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

39. ACUTE or CHRONIC PYELONEPHRITIS?

40. ACUTE or CHRONIC PYELONEPHRITIS?
Pitting geographic “scars” is the hallmark of chronic pyelonephritis.
ACUTE or CHRONIC PYELONEPHRITIS?

41. ACUTE or CHRONIC PYELONEPHRITIS?
“THYROIDIZATION” is another common hallmark of chronic pyelonephritis.
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
ACUTE or CHRONIC PYELONEPHRITIS?

42. FACTORS OBSTRUCTION: Congenital or Acquired INSTRUMENTATION
VESICOURETERAL REFLUX
PREGNANCY
AGE, SEX, why sex? F>>>M
PREVIOUS LESIONS
IMMUNOSUPPRESION or IMMUNODEFICIENCY
What are the 3 parts of the ureter which are most subject to obstruction or stones for anatomic reasons alone?
UPJ, pelvic brim, bladder inlet

43. NORMAL

44. 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
Is it fair to say just about all of the primary vascular diseases of the kidney might result in hypertension” Answer: YES

45. 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

46. 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
Does the name “malignant” imply, perhaps, EXTREME blood pressure elevations? Answer: YES

47. What is “onion-skinning”? What is “fibrinoid” necrosis?
What is an onion?
What is “fibrinoid” necrosis?

48. RENAL INFARCTS WEDGE SHAPED WELL DELINEATED “WHITE” (anemic) INFARCT
Perhaps a little “YELLOW”
HEAL WITH A SCAR
What is an “anemic” infarct? Ans: It is an infarct which is grossly pale in the acute stage because of lack of collateral circulation.

51. OBSTRUCTIONS UROLITHIASIS CONGENITAL PROSTATE ENLARGEMENT TUMORS
INFLAMMATION
SLOUGHED CLOTS, PAPILLAE
PREGNANCY
NEUROGENIC
The principle of ANY bodily tubular obstruction is that the part UPSTREAM from the obstruction may have increased pressure or become, therefore, dilated.
The part DOWN stream from the obstruction does not get fed and therefore can become atrophic, necrotic, or inflamed.
This is a CLASSICAL powerpoint slide where you are, once again, being asked to THINK like a pathologist!

52. UROLITHIASIS CALCIUM (OXALATE or PHOSPHATE) 70%
MAGNESIUM AMMONIUM PHOSPHATE 20%
URIC ACID 10%
CA↑↑↑
Bact.
U.A. ↑↑↑
What is a “staghorn” calculus?

53. TUMORS BENIGN MALIGNANT Papillary Adenoma (SIZE very important)
Fibroma/Hamartoma
Angiomyolipoma
Oncocytoma (very red, granular, mitochondria)
MALIGNANT
Renal Cell Carcinoma (Clear Cell Carcinoma, Adenocarcinoma, Hypernephroma)
Urothelial (Transitional)

54. 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?
Hematuria and pain are the two commonest symptoms, but there are NO consistent reliable early symptoms usually.
Would a urothelial (transitional pelvic) carcinoma be more likely to produce hematuria early than a clear cell? Ans: YES

55. Gross & Microscopic, Show the tumor
Gross & Microscopic, Show the tumor. Clear cell carcinoma nuclei classically look “benign”, i.e., small, uniform, centrally located.
What does YELLOW on gross and CLEAR on micro mean? Answer: FAT