Renal pathology

A/W Hypercpagulable state??

Azotemia
Infections.
Normal histology of Glomerulus.
PSGN

Children, 2w after skin or pharynx strep infection.

Type 3 HSR.
RPGN (Crescentic)
Poor prognosis.

Hematuria and Hemoptysis Tx with Emergent Plasmapheresis.

No Upper airway involvement.
DPGN
May present as Nephritic or Nephrotic.
IgA Nephropathy.

2-3 days after URI.

Alport syndrome.

Affects eye (Retina and Lens), Glomerulonephritis, Sensorineural hearing loss.

Basket weave appearance on EM.
MPGN

A/W HCV, HBV

FSGS

MCC of nephrotic syndrome in African American and Hispanics.

Minimal change
Membranous nephropathy.

Most common Nephrotic in Caucasians.

Might be Primary.
Amyloidosis.
Diabetic Nephropathy.
Kidney stones

Presentation: Flank pain and tenderness radiating to the groin. Hematuria.

Complications Hydronephrosis, Pyelonephritis.
Most important treatment FLUIDS.
Citrate in urine is protective.
Low PH favors most stones except Struvite and Calcium phosphate.
All are Radioopaque except Uric acid and Cystine stones.
Calcium stones.

CaPO4 High PH
Ca-Oxalate Low PH.
Envelope or dumbbell shaped.

CaPO4 are mainly due to hyperPTH.

Ethylene glycol Oxalic acid

Vit C Acidic urine
Crohns disease Bile fat binds calcium Increased Oxalate
absorption.
In ca-Oxalate.. Hypercalcemia is not a must.
Tx: Fluids, Thiazide, Citrate.
Ammonium Magnesium Phosphate.
Struvite.

Tx with A.biotics and Surgery.

Uric acid stone

Visible on CT and US but not X-ray.

A/W Hyperuricemia. (gout and leukemia)
Tx: Alkalanization of urine. Allopurinol
Cystine stone

Hexagonal.

AR. Defect in PCT cysteine absorption.

A child with recurrent kidney stones and Staghorn Calculus!
Tx: Alkaline the urine!
Hydronephrosis.

Distention and dilation of renal pelvis and Calyces

Causes: Any obstruction Stones, BPH, Cancer,
Retroperitoneal fibrosis, VUR.
Serum Cr (renal function) will be elevated if single kidney or bilateral.
Renal system Cancers.

Kidney (Cortex medulla (nephrons)) Columnar epithelium.

Renal tract From Calyces until bladder. (Transitional epithelium)
Transitional epithelium can convert to Sq. epithelium due to chronic
irritation.
 RCC (MC renal malignancy
Originates from PCT Polygonal Clear cells, Why?
Filled with Lipids and Carbs.
MC in old men who are smokers/Obese.

Presentation: Hematuria, Casts, Polycythemia! Flank pain, mass and weight

loss .. Usually silent until metastasis.

Invades renal vein IVC Bones and lungs. (Hematogenous)

Tx with surgery if local...Immune therapy if Mets Chemo and radio
resistant.
Renal oncocytoma.

Benign epithelial tumor. Well circumscribed.

Eosinophilic cells with abundant Mitochondria without Neuclear clearing (Vs
RCC).
Presentation similar to RCC. Without Paraneoplastic syndromes.
Tx: Resection to RO RCC.
Wilms Tumor. MC malignant tumor in
children.

Contains embryonic glomerular structure.

MC presentation Large palpable painless abdominal mass while bathing.

Important associations:
TCC

MC cancer of Renal tract (Calyces Bladder)

MC presentation painless hematuria without Casts!
Painless Hematuria next step?? Cystoscopy.

MC side effect of cyclophosphamide hemorrhagic cystitis.

SCC
UTI

MCC E.Coli.
Ranges from Urethritis (Gonnorrhea, Chlamydia) cystitis (bladder), no
systemic symptoms or Pyelonephritis (Kidney), Systemic symptoms.
Treatment antibiotics.
 Acute cystitis

Inflammation of urinary bladder.

Diagnoses Urine analysis for WBCs and Gram stain

Followed by culture.

Important.
Acute Pyelonephritis

Neutrophils infiltrating Cortex (Spares glomeruli and vessels)

And Chills.
Either due to Ascending UTI or hematogenous.
Labs: WBCs + Casts.
CT shows striated parenchyma.
Chronic Pyelonephritis.

Recurrent acute due to Predisposing factor (VUR, Stone)

Drug induced interstitial nephritis.
(Tubulointerstitial)
Drug reaction.
Eosinophilurea, Fever and Rash. + Azotemia and hematuria.
Type 3 HSR (A.B + Drug) 1-2 w after drug.

Diffuse Cortical necrosis.

Diffuse bilateral kidney infarction.

Bilateral flank pain.
Due to
ATN.

Sudden injury to renal tubules Renal tubules lose their functions. High
FeNa
Usually transient and reversible but might lead to death.

Composed of?

Ischemia or toxin

2nd phase is the most dangerous and has the highest risk of death.
Causes:

Ischemia. Anything that causes hypotention and decreased RBF Death of

tubular cells that fall in lumen.
PCT and thick ascending limbs are highly susceptible. Why???
Renal papillary necrosis.

Sloughing of renal papilla. Hematuria, Proteinuria

May be triggered by infection or immune stimulus.
Phenacitin
AKI (Previously called ARF)

Abrupt Decline in Kidney function High BUN and Cr.

Prerenal Vs Renal Vs postrenal
Prerenal Azotemia.

Hypotention Low RBF low GFR Na/H2O/BUN retention to preserve

volume. Cr is not absorbed! High BUN/Cr ratio.
FeNa <1% (Normal)
If hypotention is severe it will lead to ATN and convert to intrarenal Azotemia.
Intrensic renal Azotemia.

ATN or Acute GN.

Granular casts block the tubule Low GFR.
Because Tubule function is not intact BUN and Sodium are not absorbed
High FeNa and low BUN/Cr.
Post renal azotemia.

BUN/Cr is high initially then it will be low.

Renal failure.

Consequence.
ADPKD.

Berry aneurism! FH of intracranial bleeding.

ARPKD
Medullary cystic disease.