Pathology Lab-Renal Flashcards
A 68-year-old man presented with low-grade fever, right flank pain and gross hematuria. He has a history of hypertension and COPD. Examination revealed a palpable flank mass. What do you want to know about the patient’s urinalysis?
Are there RBC casts? This would indicate origin of bleeding as downstream from the glomerulus.
A 58-year-old black male with a 4-year history of hypertension now presents with an elevated BUN and creatinine. Physical examination reveals a bilateral palpable abdominal masses. What would you estimate this patient’s GFR is?
When BUN and creatinine are elevated you are at end-stage renal disease which is around 15-20mL/min.
A male infant developed respiratory distress a few minutes following delivery and expired after 3 hours of extrauterine life in spite of aggressive resuscitation. The pregnancy was complicated by oligohydramnios; a fetal ultrasound disclosed bilateral renal masses. The gross image of the child’s kidney is shown below. How is this condition different from autosomal dominant polycystic kidney disease?
Note that the cysts are perpendicular to the capsule and cylindrical. This is because the collecting ducts (seen below) are dysfunctional in AR PKD. In AD PKD the cysts can occur anywhere in the kidney.
A 73-year-old man presented with a creatinine of 4.3 mg/dL. He had been treated for hypertension for 15 years but was otherwise in good health. Examination revealed an enlarged prostate. What is likely responsible for the elevated creatinine levels seen in this patient’s blood?
Blockage by the prostate causes back-up of urine and increases the pressure in Bowman’s capsule and filtration decreases.
A 59-year-old man is admitted after a cardiac arrest secondary to acute myocardial infarction. He does well initially, but 3 days later his urine output drops and his creatinine rises to 4.8 mg/dL. What is responsible for this patient’s increase in blood creatinine?
Acute tubular necrosis. The drop in pre-renal perfusion causes ischemia and tubular cells die.
A 62-year-old man presented with history of benign prostatic hyperplasia and multiple urinary tract infections. He died of unrelated causes. Gross specimen is shown below. How might you have been able to see this on ultrasound?
Hydronephrosis and no delineation between the cortex and the medulla. On histology you would expect to see loss of tubules, streams of inflammatory cells,
What is the most common genetic abnormality seen with the condition seen below?
VHL, a tumor suppressor gene, lost on the p3 arm of the chromosome causes clear cell renal carcinoma.
What about this image is a “slam-dunk” diagnosis for renal cell carcinoma?
Orange-yellow mass mixed with the vasculature areas.
Why is hematuria the most common presentation with renal cell carcinoma?
Hematuria. The tumors are very vascular.
What makes renal cell carcinoma have its yellowish appearance?
The clear cells typical of this tumor are filled with lipid.
A patient presents to the operating room to get his kidney taken out because he has renal cell carcinoma. What is the prognosis for this patient after viewing his kidney seen below?
Note renal vein and perinephric fat invasion. This lowers the prognosis significantly due to metastasis.
What are the most common sites of metastasis for renal cell carcinoma?
Bone and lung. Note the image on the right is also a metastasis to the testicle.
A patient presents to your clinic complaining of right flank pain and hematuria. Physical exam reveals a palpable mass on the right side of the patient. Biopsy of the mass is seen below. What genetic abnormality is associated with this condition?
MET-protoncogene is involved in papillary renal cell carcinomas.
A 71 year old male presents with hematuria and right flank pain. He has a palpable left-sided mass. Biopsy of the mass is shown below. What type of renal cell carcinoma is this? Where do these originate from? What is the prognosis?
This is a chromophobe renal cell carcinoma. They come from the collecting ducts. These only make up about 5% of renal cell carcinomas. Note the well defined cellular borders.
Which renal cell carcinomas come from the renal tubular epithelium?
Clear cell and papillary comes from renal tubular epithelium
What paraneoplastic syndromes present with renal cell carcinoma?
EPO = polycythemia, Renin = hypertension, PTHrP = hypercalcemia, ACTH = Cushing’s
What other conditions are associated with the condition seen below?
Berry aneurisms, mitral valve prolapse and liver cysts.
What drugs do you not want to give a patient with PKD?
NSAIDs, blood thinners or anything that will raise the blood pressure. The last thing you want is to cause bleeding in the patient’s kidney.
Why do you need to treat UTIs more aggressively in patients with PKD?
As the disease progressed there is increased compression of renal collecting ducts (seen below) and urinary stasis. This can be a fertile environment for infection.
Why does mutation of PKD1 and PKD2 cause cyst formation?
Normally the cilium senses and signals tubular flow in the kidney. In PKD, abnormal signaling from the cilium causes the epithelial cells to secrete fluid and proliferate.
What other organ is commonly affected in infants with AR PKD?
The liver tends to see fibrosis, especially around the portal tract as seen below.
What gene is responsible for AR PKD?
PKHD1 that encodes for fibrocystin.
What are potential causes of oligohydramnios?
Bilateral renal agenesis, leaky amniotic membranes and urethral atresia (seen below).
What is Potter’s sequence?
Abnormal facies, shortened extremities and pulmonary hypoplasia.
What causes pulmonary hypoplasia in kids with oligohydramnios?
Anything that puts pressure on the chest (enlarged bladder seen below) wall and impedes development of the lungs.
What different things can cause urinary obstruction?
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What infection puts you at risk for developing kidney stones?
Proteus mirabilis makes urease which creates a more alkaline urine.
When do you know patients have recovered from acute tubular necrosis from ischemia?
Polyuria
What is different about acute tubular necrosis from nephrotoxins?
You do not get oliguria
Which of these histological images below indicates acute tubular necrosis? Why?
The one on the bottom. Note the anucleate tubular cells that have fallen into the actual tubular lumen and spacing between the tubules from edema.
What is produced in the urine of patients with acute tubular necrosis?
Epithelial casts (seen below)
What can cause the condition seen in the kidney slice seen below?
This is chronic pyelonephritis. Note the atrophy and dilation of the renal pelvis.
A 9-year-old boy was diagnosed with streptococcal sore throat. One week later he was admitted to the hospital with edema of the face and feet with a blood pressure of 140/100. He gradually became oliguric. Urinalysis revealed Sp Gr 1.010, 2+ protein, many WBCs and RBCs, hyaline, granular and numerous. RBC casts in the sediment. What is causing this patient’s symptoms?
Post-streptococcal glomerulonephritis. Note the hypertension, oliguria and casts in urine indicating a nephritis. Group A strep infection is indicated in his history.
A 68-year-old man was admitted with weakness, productive cough of bloody mucoid sputum, shortness of breath and weight loss of about one month’s duration. He had also noticed dark-brown urine. Labs: Anemia with a normal differentiation was noted. Urinalysis revealed Sp Gr 1.010, 4+ protein, numerous RBC, WBC, RBC casts and hyaline casts. BUN was 80 mg/dL and creatinine 5.0 mg/dL. Ancillary Studies: Chest X-ray revealed bilateral pulmonary fibrocystic changes. What are your first two differentials in this patient?
This patient has rapidly progressive glomerulonephritis (RPGN). The presence of lung pathology leads you to Goodpasture’s syndrome or Wegener’s granulomatosis.
A 3-year-old boy developed nephrotic syndrome at the age of 2 1/2. He was treated with Prednisone and did well for five months when edema and proteinuria recurred. Labs: Urinalysis showed Sp Gr 1.030 and 4+ protein. The 24-hour urinary protein excretion was 6 g. The serum cholesterol was 630 mg/dL and the serum albumin was 1.7 g/dL. What conditions can cause nephrotic syndrome in a young child?
Minimal change disease (most common in kids), focal segmental glomerulosclerosis (most common in adults), membranous glomerulopathy, diabetic glomerulosclerosis or amyloid.
A 60-year-old man with a long history of hypertension presented with progressive edema of the lower extremities and severe proteinuria (7.7 g/day). Labs: Urinalysis revealed Sp Gr 1.030, 4+ protein, hyaline and granular casts. Serum albumin was 1.8 g/dL, cholesterol 410 mg/dL, BUN 33 mg/dL and creatinine 1.8 mg/dL. Renal biopsy is shown below. What is your diagnosis? What would you see if you used a silver stain?
Note very thick loops and walls indicated on Masson’s trichrome stain. Note the absence of hypercellularity or RBCs. This is membranous glomerulonephropathy. Silver stain would reveal unstained pink “spike-like) immune complexes covered by epithelium in the GBM.
During a routine U.S. Army medical induction examination, a 21-year-old recruit was found to have mild hypertension, microscopic hematuria and 2+ protein. He also reported mild flank pain and some flu-like symptoms several days earlier. Immunofluorescence reveals IgA antibody. Where would you see most of the damage occurring in the glomerulus?
IgA immune complexes typically affects the mesangium more than the capillary loops. Note the extra pink (mesangium), areas of mesangial sclerosis and red-staining collections of IgA (arrow).
A 76-year-old man had a long history of diabetes mellitus. He was admitted with metastatic prostatic carcinoma, chronic renal failure and expired. At autopsy, the kidneys are noted to be irregularly scarred. The cortex is contracted. The renal papillae of the left kidney are blunted, yellow, soft and show focal hemorrhage. What would you expect to see on renal biopsy of this patient?
Non-enzymatic glycosylation of glomerular walls disrupts the glomerulus’s ability to filter by causing intense thickening from matrix deposition (Kimmelstiel-Wilson deposits) and arteriolosclerosis (arrow).
What does a healthy glomerulus look like?
Absent of neutrophils, low cellularity in tufts (7-8 mesangial cells), thin parietal epithelial cells and minimal spacing between tubules.
A 9-year-old boy was diagnosed with streptococcal sore throat. One week later he was admitted to the hospital with edema of the face and feet with a blood pressure of 140/100. He gradually became oliguric. Urinalysis revealed Sp Gr 1.010, 2+ protein, many WBCs and RBCs, hyaline, granular and numerous. RBC casts in the sediment. How would you expect his renal biopsy to appear?
Diffuse glomerulonephritis with hyper cellular (neutrophil, mesangial cell and epithelial cell proliferation) and enlarged glomeruli.
A 9-year-old boy was diagnosed with streptococcal sore throat. One week later he was admitted to the hospital with edema of the face and feet with a blood pressure of 140/100. He gradually became oliguric. Urinalysis revealed Sp Gr 1.010, 2+ protein. What would you expect to see if you looked at the patient’s urine under a microscope?
RBC and WBC casts.
A 9-year-old boy was diagnosed with streptococcal sore throat. One week later he was admitted to the hospital with edema of the face and feet with a blood pressure of 140/100. He gradually became oliguric. Urinalysis revealed Sp Gr 1.010, 2+ protein, many WBCs and RBCs, hyaline, granular and numerous. RBC casts in the sediment. What would you expect to see on EM of the patients glomeruli?
Subepithelial immune complex deposits “humps”
A 9-year-old boy was diagnosed with streptococcal sore throat. One week later he was admitted to the hospital with edema of the face and feet with a blood pressure of 140/100. He gradually became oliguric. Urinalysis revealed Sp Gr 1.010, 2+ protein, many WBCs and RBCs, hyaline, granular and numerous. RBC casts in the sediment. His immunofluorescence is shown below. What causes the image to appear the way it does?
Early PSGN starts in the mesangium and then moves to the basement membrane. This will create a granular immunofluorescence.
What type of immune deposition does not elicit neutrophil response or mesangial damage.
Membranous glomerulopathy. Immune complexes bypass the mesangium and go straight to the basement membrane.
A patient comes to see you with pulmonary and renal problems. Immunofluorescence is shown below. What is your diagnosis?
In Goodpasture’s antibody against type IV collagen coats the basement membrane in the lungs and in the kidney. This will show up as linear immune complex deposits along the basement membrane.
A 68-year-old man was admitted with weakness, productive cough of bloody mucoid sputum, shortness of breath and weight loss of about one month’s duration. He had also noticed dark-brown urine. Labs: Anemia with a normal differentiation was noted. Urinalysis revealed Sp Gr 1.010, 4+ protein, numerous RBC, WBC, RBC casts and hyaline casts. BUN was 80 mg/dL and creatinine 5.0 mg/dL. Ancillary Studies: Chest X-ray revealed bilateral pulmonary fibrocystic changes. What would you expect to see on renal biopsy of this patient?
In RPGN the parietal cells proliferate and cause crescentic fibrosis. You would also see neutrophils and blood in the tubules.
What are the different types of rapidly progressive glomerulonephritis?
Type I: Anti-GMB antibody, Type II: Immune complexes, Type III: Pauci-Immune
How do you further classify pauci-immune glomerulonephritis?
c-ANCA: Wegener’s, p-ANCA: Microscopic polyangiits. 90% of idiopathic cases also indicate p or c ANCA.
A 3-year-old boy developed nephrotic syndrome at the age of 2 1/2. He was treated with Prednisone and did well for five months when edema and proteinuria recurred. Labs: Urinalysis showed Sp Gr 1.030 and 4+ protein. The 24-hour urinary protein excretion was 6 g. The serum cholesterol was 630 mg/dL and the serum albumin was 1.7 g/dL. What would you expect to see on renal biopsy of this patient?
MCD. Proteinaceous fluid in tubules, normal glomeruli and foamy PCT cells due to lipid reabsorption (liver overcompensates with lipid secretion due to loss of albumin)
A 3-year-old boy developed nephrotic syndrome at the age of 2 1/2. He was treated with Prednisone and did well for five months when edema and proteinuria recurred. Labs: Urinalysis showed Sp Gr 1.030 and 4+ protein. The 24-hour urinary protein excretion was 6 g. The serum cholesterol was 630 mg/dL and the serum albumin was 1.7 g/dL. What would you expect to see on EM of this patient’s glomerulus?
MCD would show effacement of the foot processes on the visceral epithelium.
What do we think minimal change disease is? What treatment would it respond to?
Immunologic abnormality that results in release of a cytokine that damages the visceral epithelium that allows protein leakage. It responds to steroids because cytokines are the culprit.
What genetic conditions predispose people to minimal change disease?
HLA genes and lymphomas
Most patients with focal segmental glomerulosclerosis have an idiopathic etiology. What puts patients at risk for FSGS?
HIV, Sickle-cell, Heroin abuse & obesity.
What is different about FSGS from MCD?
FSGS does not respond to steroids, does not regress and results in renal failure. MCD does respond to steroids and typically regresses with full recovery.
A 60-year-old man with a long history of hypertension presented with progressive edema of the lower extremities and severe proteinuria (7.7 g/day). Labs: Urinalysis revealed Sp Gr 1.030, 4+ protein, hyaline and granular casts. Serum albumin was 1.8 g/dL, cholesterol 410 mg/dL, BUN 33 mg/dL and creatinine 1.8 mg/dL. EM of renal biopsy is shown below. How does this condition cause damage to capillary walls?
Note the subepithelial “spike and dome” of immune complex typical of membranous glomerulonephropathy. Deposition of immune complex does not cause direct inflammation. It activates the part of complement that forms pores, lyses cells and releases materials that damage the capillary walls.
A 60-year-old man with a long history of hypertension presented with progressive edema of the lower extremities and severe proteinuria (7.7 g/day). Labs: Urinalysis revealed Sp Gr 1.030, 4+ protein, hyaline and granular casts. Serum albumin was 1.8 g/dL, cholesterol 410 mg/dL, BUN 33 mg/dL and creatinine 1.8 mg/dL. EM of renal biopsy is shown below. How would you expect this patient’s immunofluorescence to appear?
This patient has membranous glomerulonephropathy. You would see discontinuous and granular immunofluorescence.
What are the causes of membranous glomerulonephropathy?
85% are idiopathic. The other 15% consist of malignancies, tumors, drugs and autoimmune diseases that can create immune complexes.
What is the most common type of glomerulonephritis in the world?
IgA Glomerulonephropathy.
Why do so many patients with IgA nephropathy go into renal failure?
It is a slowly progressing disease.
What is the most common population affected by IgA nephropathy?
Young adult males
A young child presents with purport, hematuria and joint pain. What is your diagnosis?
A systemic vasculitis associated with a more extreme form of IgA nephropathy in kids…Henoch-Schonlein.
A 76-year-old man had a long history of diabetes mellitus. He was admitted with metastatic prostatic carcinoma, chronic renal failure and expired. At autopsy, the kidneys are noted to be irregularly scarred. The cortex is contracted. What histologic pathologies are associated with diabetes?
Glomerulosclerosis, arteriosclerosis and papillary necrosis.
What conditions cause papillary necrosis?
Diabetes, analgesic nephropathy, obstruction w/infection and sickle cell.
