Notes on Kidney Disorders

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Findings in renal dysfunction:

• Hematuria, proteinuria.

Renal function tests:

Blood urea nitrogen (BUN):

• End product of amino acid and pyrimidine metabolism.

• Produced by liver.

• Increased in CHF.

Serum creatinine:

• Metabolic end product of creatine in muscle.

• 100% filtered; none absorbed; none secreted.

• Increased by creatine supplements.

BUN/Creatinine ratio:

• Normal is less than 15.


• Increased BUN and creatinine levels.


• Causes: decreased CO.


• Causes: parenchymal damage to kidneys; tubular necrosis, renal failure.


• Causes: urinary tract obstruction below kidneys.

Renal function tests:

Creatinine clearance:

• Correlates with GFR.

• Detects renal dysfunction.

• Increased in pregnancy; decreased in elderly people, renal disease, etc.


• Detection of renal disease.


• GBM: type IV collagen; size and charge determine filtration.

• GBM may be thickened by deposition of immunocomplexes and increased type IV collagen.

Immunofluorescence stain:

• Linear pattern: anti-GBM disease, eg., Goodpasture syndrome.

• Granular (lumpy-bumpy) pattern: immunocomplex deposition on glomerulus.

Glomerular disease:

• Immunocomplexes (type III hypersensitivity).

• Antibodies against GBM, eg., Goodpasture syndrome.

Nephritic syndrome:

• Hypertension, periorbital puffiness, oliguria, hematuria, neutrophils in the sediment.

• RBC casts; proteinuria, azothemia.

Nephrotic syndrome:

• Increased proteinuria.

• Pitting edema, ascites.

• Hypoalbuminemia.

• Infections, eg., S. pneumoniae.

• Hypertension, hypercoagulability, hypercholesterolemia, hypogammaglobinemia, fatty casts.

Systemic diseases associated with nephrotic syndrome:

Diabetic glomerulopathy:

• Nodular glomerulosclerosis, Kimmelstiel-Wilson disease.

• Nonenzymatic glycosylation (NEG) of GBM.

• Nonenzymatic glycosylation of afferent and efferent arterioles.

• Osmotic damage.

• Hyperfiltration.

• Diabetic microangiopathy = Increased deposition of type IV collagen.


• Microalbuminuria.

Alport's syndrome:

• XD disease.

• Defective GBM collagen synthesis.

• Foam cells.

• Hematuria.

Chronic glomerulonephritis:

• Shrunken kidneys, sclerosis and tubular atrophy.

Acute tubular necrosis:

Acute renal failure:

• Causes: acute tubular necrosis, obstruction, vascular disease, RPGN, DIC, drugs.

Ischemic acute tubular necrosis:


• Azothemia.


• Obstruction, decreased GFR, oliguria.

Tubulointerstitial nephritis:

• Inflammation of tubules and interstitium.


• Acute pyelonephritis, drugs, infections, SLE, lead poisioning.

Acute pyelonephritis:


• Urinary tract obstruction, medullary sponge kidney, diabetes mellitus, pregnancy, sickle cell disease.

• Vesicoureteral reflux with ascending infection.

• Ascending infection = most common mechanism for UTIs in females.

• Spiking fever, flank pain, increased frequency of urination.

• WBC casts, pyuria, bacteriuria.


• chronic pyelonephritis, perinephric abscess, renal papillary necrosis, septicemia, shock.

Chronic pyelonephritis:

• Lower urinary tract obstruction.

• Had a history of acute pyelonephritis.


• Penicillin, rifampin, NSAIDs, sulfonamides, diuretics.

• Type I and IV hypersensitivity.

• Fever, oliguria, rash.

• BUN:Cr ratio less than 15.

Analgesic nephropathy:

• Occurs in patients with chronic pain.

• Acetaminophen free radicals damage renal tubules in medulla.

• Chronic use of acetaminophen + aspirin.

• No PGE2; unopposed ATII.


• Renal papillary necrosis, hypertension, CRF, renal pelvic/bladder transitional cell carcinomas.

Urate nephropathy:

• Urate crystal deposition in tubules and interstitium.

• Give patients allopurinol before chemotherapy.

• Caused by: purines, lead poisoning, gout.

Chronic lead poisoning:

• Decreased secretion of uric acid.

• Tubulointerstitial nephritis.

Multiple myeloma:

• Bence Jones proteinuria.

• Nephrocalcinosis.

• Amyloidosis with nephrotic syndrome.

Fractional excretion of Na:

• Less than 1% = good tubular function.

• Greater than 2% = tubular dysfunction; risk for acute tubular necrosis.

Chronic renal failure:

• Irreversible azotemia.

• End stage renal disease.

• Causes: diabetes mellitus, hypertension, glomerulonephritis, cystic renal disease.

• Small shrunken kidneys.

• Anemia, defective platelets.

• Renal osteodystrophy: osteitis fibrosa cystica, osteomalacia, osteoporosis.

• Hypertension, pericarditis, CHF, atherosclerosis.

• Gastritis, uremic frost.

• Hyperkalemia + anion gap metabolic acidosis.

• Hypocalcemia; hypovitaminosis D; hyperphosphatemia.

• Urine lacks concentration and dilution; waxy and broad cysts seen.

Vascular disorders:

BNS: Benign nephrosclerosis:

• Due to essential hypertension.

• Small kidneys.

• Proteinuria, hematuria, azotemia.

Malignant hypertension:

• Sudden hypertension.

• Causes: BUN, HUS, TTP, systemic sclerosis.

• Vascular damage to arterioles and small arteries.

• Flea-bitten kidneys, onion skin lesions.


• Hypertension, renal failure, encephalopathy.

• Lab: azotemia, hematuria, proteinuria.


• Sodium nitroprusside.

Renal infarction:

Causes: Thrombus embolization in left heart.

• Atheroembolic renal disease.

• Vasculitis.

• V-shaped infarcts.

• Sudden pain and hematuria.

Sickle cell nephropathy:

• Occurs in sickle cell patients.

• Hematuria, lack of concentration, necrosis, pyelonephritis.

Diffuse cortical necrosis:

• Obstetric emergency complication.

• DIC.

• Anuria.

Obstructive disorders:


• Due to: Renal stone, retroperitoneal fibrosis, cervical cancer, BPH.

• Azotemia.

Renal stones: urolithiasis:

• Due to: hypercalciuria, concentrated urine, reduced urine citrate, hyperparathyroidism, high dairy products, infection (eg., Proteus). Types of stones:

• Calcium oxalate = vegans + Crohn's; calcium phosphate = dairy products + tubular acidosis, magnesium ammonium phosphate, uric acid, cystine.


• Ipsilateral colicky pain, hematuria.



• Hamartoma.

• Associated with tuberous sclerosis.

Renal cell carcinoma:

• Alias Grawitz tumor, clear cell carcinoma, hypernephroma.

• Smoking, VHL, adult polycystic kidney disease.

• Metastasis to lungs.

• Cannonball appearance.

• Lytic lesions.

• Hemorrhagic lesions.


• Hematuria, flank mass, costovertebral angle pain.

• Ectopic secretion of: erythropoietin, PTH-related protein.

Cancers of renal pelvis:

Transitional cell carcinoma:

• Most common.

• Smoking, phenactin abuse, aromatic amines, cyclophosphamide.

Squamous cell carcinoma:

• Renal stones, infection.

Wilm's Tumor:

• 2-5 years of age.

• AD disease; chromosome 11.

• WAGR syndrome: Wilm's tumor, aniridia, genital abnormalities, retardation.

• Beckwith-Wiedemann syndrome.

• Unilateral palpable mass; hypertension.

• Metastasis to lungs.

Additional Reading:

Basic Pathology

1. Cell Injury
2. Inflammation and Repair
3. Immunopathology
4. Water, Electrolyte, Acid-Base, Hemodynamic Disorders
5. Genetic and Developmental Disorders
6. Environmental Pathology
7. Nutritional Disorders
8. Neoplasia
9. Vascular Disorders
10. Heart Disorders
11. Red Blood Cell Disorders
12. White Blood Cell Disorders
13. Lymphoid Tissue Disorders
14. Hemostasis Disorders
15. Blood Banking and Transfusion Disorders
16. Upper and Lower Respiratory Disorders
17. Gastrointestinal Disorders
18. Hepatobiliary and Pancreatic Disorders
19. Kidney Disorders
20. Lower Urinary Tract and Male Reproductive Disorders
21. Female Reproductive and Breast Disorders
22. Endocrine Disorders
23. Musculoskeletal Disorders
24. Skin Disorders
25. Nervous System Disorders
26. Notes on Tissue Regeneration
27. A Table of Bleeding Disorders
28. FAQ on Structure and Function of Red Blood Cells
29. FAQ on Components of Blood
30. Notes on Hemostatic Mechanisms
31. What is Fever?
32. What is Edema?
33. FAQ on Blood Pressure
34. FAQ on principles of fluid and flow dynamics of Blood
35. Causes of Thrombocytopenia
36. Squamous cell carcinoma of head and neck mucosa
37. Four tumors which never metastasize to the brain
38. What is caustic injury?
39. What causes Peripheral Edema?

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