The human kidney is a product of the metanephric system. Recall, pronephros, mesonephros, metanephros, woolffian, muellerian.
Sallow = 196, 145, 141 (RGB)
Mutations in EYA1 or SIX1 genes have been associated with multicystic renal dysplasia.
How many kidneys in your cadaver lab had NO cysts whatsoever? Probably not many?
Even though there are MANY types of glomerulonephropathies, here are some of the common findings seen in many of them.
Here is the warzone of the glomerulopathies: 1) podocytes, 2) basement membrane, 3) endothelium
Why is the pic on the left classic for glomerulonephritis? Ans: Inflammatory cell infiltrates in the glomeruli
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.
To make a long story short, the NEPHROTIC SYMDROME is usually a sign of a glomerulonephropathy.
What does indolent mean? “Causing little or no pain; inactive or relatively benign”
The ability to recognize the BM as being rather uniform in thickness and density is so critically important
Once again, as in “chronic” pancreatitis, the main features of “chronic” are more a fibrosis (hyalinization), rather than lymph and macrophage infiltrates.
What percentage of these tubules are PROXIMAL convoluted tubules rather than DISTAL? Answer: 98%
The “necrotic” tubular cells are karryolytic.
Pitting geographic “scars” is the hallmark of 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
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
Is the primary inflammatory focus in the tubules or interstitium BETWEEN the tubules?
What is “metastatic” calcification? Ans: The tissue calcification due to hypercalcemia
Differentiate Bence-Jones protein from amyloid
Is it fair to say just about all of the primary vascular diseases of the kidney might result in hypertension” Answer: YES
Does the name “malignant” imply, perhaps, EXTREME blood pressure elevations? Answer: YES
Could fibrin plugs in small vessels easily be missed if a fibrin stain is not done, thinking this is merely blood? Answer: YES
Is the CORTEX of a kidney MUCH more susceptible than a MEDULLA to ischemia? Answer: YES
What is an “anemic” infarct? Ans: It is an infarct which is grossly pale in the acute stage because of lack of collateral circulation.
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!
What is a “staghorn” calculus?
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 Why are oncocytes very RED and granular?
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
Angiogram, CT, Gross, Microscopic, respectively. Show the tumor in each one. 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
The most likely place for a transitional (urothelial) carcinoma, is smack dab in the HILUM! (because that’s where the transitional mucosa is)
Drugs, Tumors, SLE, Infections
Deposition of Ag-Ab complexes
Indolent, but >60% persistent proteinuria
15% go on to nephrotic syndrome
MINIMAL CHANGE GLOM.
• MOST COMMON CAUSE of
NEPHROTIC SYNDROME in CHILDREN
• EFFACEMENT of FOOT PROCESSES
• Just like its name
– Glomerulo-SCLEROSIS (NOT
• HIV, Heroine, Sickle Cell,
• Most common cause of
ADULT nephrotic syndrome
• MPGN can be idiopathic
or 2º to chronic immune
diseases Hep-C, alpha-1antitrypsin, HIV,
• GBM alterations, subendo.
• Leukocyte infiltrations
• Predominant MESANGIAL
• Mild hematuria
• Mild proteinuria
• IgA deposits in mesangium
• 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
• Can result from just about ANY
of the previously described
– THIN CORTEX
– HYALINIZED (fibrotic) GLOMERULI
– OFTEN SEEN IN DIALYSIS
ACUTE TUBULAR NECROSIS
Destruction of renal TUBULAR epithelium
Loss of renal function
50% of ACUTE renal failure
• 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
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
RENAL CELL CARCINOMA
• TOBACCO RELATED, STRONGLY
• SOME HEREDITARY/FAMILIAL
• MOST are “CLEAR CELL”, a few
• YELLOW grossly, “CLEAR” cells
• STRONGLY tend to invade the renal
VEIN early, in preference to lymphatics.
Does the kidney have lymphatics?
• 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
• Associated with ureter and bladder