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BOARD REVIEW. NEPHROLOGY 1. URINALYSIS. Proteinuria 1) overflow of proteins- MM, MGUS 2) increased filtration of proteins: glomerular diseases: nephrotic protein> 3g/day nephritic protein<2 g/day 3) decreased tubular reabsorbtion: tubulointerstitial nephritis: protein< 2g/day

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Board review




  • Proteinuria

  • 1) overflow of proteins- MM, MGUS

  • 2) increased filtration of proteins: glomerular diseases: nephrotic protein> 3g/day

  • nephritic protein<2 g/day

  • 3) decreased tubular reabsorbtion: tubulointerstitial nephritis: protein< 2g/day

  • 4) transient: fever, exercise, upright position, seizures


  • Normally< 100 mg proteins excreted daily

  • Normally < 30 mg albumin excreted daily

  • Microalbuminuria 30-300 mg daily seen in early DM nephropathy

  • 1. patient with fever and UTI, urine + for protein wtd?

  • 2. patient on NSAIDs for pain. UA + for protein wtd?

  • 3. patient with proteinuria on dipstick after exercise wtd?


  • Casts:

  • Nephrotic sdr hyaline casts, fatty casts, oval fat bodies

  • Nephritis RBC casts

  • Pre-renal azotemia hyaline casts

  • ATN muddy/ dirty brown, pigmented casts

  • Interstitial nephritis WBC casts, granular casts, eosinophils

  • Chronic renal failure chronic renal failure


  • 1. Eosinophiluria can be seen in the following except:

  • A) interstitial nephritis

  • B) athero embolism

  • C) NSAIDs

  • D) rapidly proliferative glomerulonephritis

  • 2. A 72 year old Asian female has anorexia, night sweats and hematuria. There is no pain or other urinary symptoms. Urine has no casts, 21 WBC. Urine culture is sterile. BUN and creatinine are mildly elevated. X ray chest is negative. What is your next step?

  • a) dsDNA ab b) PPD c) CT scan chest d) renal bx


1. hyaline casts

2. muddy brown casts

3. RBCs

4. RBC casts

5. Oval fat bodies

6. eosinophils


B. prerenal azotemia

C. glomerulonephritis

D. nephrolithiasis

E. interstitial disease

F. nephrotic syndrome



  • 1) calcium oxalate crystals: envelope appearance-acid urine- ethylene glycol toxicity, intestinal hyperoxaluria( ex. Chron)

  • 2) cystine crystals( hexagonal shaped, positive urine nitroprusside test), in cystinuria ( patient young, around 20)

  • 3. uric acid crystals- in acid urine- tumor lysis sdr

  • 4. calcium phosphate crystals (needle like prismatic)- in alkaline urineeg distal RTA, idiopathic hypercalciuria, primary hyperparathyroidism

  • 5. struvite stones- staghorn, MgNH4Po4(coffin lids) in alkaline urine- UTi with urease producing bacteria

Renal failure
Renal failure

  • Pre-renal azotemia- decreased renal perfusion

  • volume depletion- bleeds, diarrhea, burns, etc

  • volume overload- CHF, cirrhosis

  • Decresed urine volume- increased urine osmol,

  • Decreased urine Na FeNa <1

  • Urine sediment neg

  • FeNa= Urine Na x plasma creatinine/ urine creatininex plasma Na X100

Intrinsic acute renal failure
Intrinsic acute renal failure

  • -Glomerular disease- urine: RBC casts

  • -ATN- aminoglycosides, ampho B, rhabdo, tumor lysis, athero embolism

  • urine- muddy brown casts

  • -tubulo interstitial disease

  • Allergic- B lactam, sulfa, dilantin, quinolone

  • NSAIDs- no eosinophils

  • Urine- WBC- eosinophils


  • 1. Elderly man with h/o HTN, DM, hyperlipidemia on beta blocker, statin, HCTZ. Blood pressure still elevated at 170/110. Serum creatinine 1.1. Patient is started on Ace inhib. One week later, BP controlled. BUN/creat 19/1.5. UA – no sediment. The most likely cause of ARD is:

  • A) tubulointerstitial disease

  • B) ATN

  • C) rhabdo sec to statin

  • D) ACE inhib

  • 2. a young man with h/o drug abuse and recent seizures presents with lab findings- BUN- 65, creatinine 5 hyperphosphatemia, hyperkalemia, high uric acid, low calcium, high CP. Urine no RBC, positive for heme. Muddy brown casts are seen. Dg?


  • 1.ATN can be caused by any of the following except:

  • A) aminoglycosides

  • B) ampho B

  • C) cyclosporine

  • D) rhabdomyolysis

  • E) NSAIDs

  • 2. Patient with post infarct angina scheduled for cardiac cath. H/o DM- serum creatinine 1.6. Best way to prevent radiocontrast nephropathy is

  • A) ½ NS 12 h pre and post procedure +/- acetylcysteine

  • B) ½ NS 6 h pre and post procedure

    C) 0.9 NS with diuresis at th end of procedure


  • 65 year old woman presents with abdominal pain and fever. Patient is started on Ampicillin, Gentamycin, Flagyl. CT scan abdominal with contrast is done. Next day patient has decreased urine output to 300cc/24h. Serum BUN/ creat 40/2.2

  • UA shows no sediment. FeNa <1.

  • The most likely diagnosis?

  • A) ampicillin induced interstitial nephritis

  • B) gentamycin induced toxicity

  • C) radiocontrast induced nephropathy

Renal effects of nsaids
Renal effects of NSAIDs

  • NSAID inhibit renal prostaglandin( PG causes vasodilation and stimulates renin secretion)

  • NSAIDs decrease renal blood flow and decrease renin secretion:

  • Prerenal azotemia

  • Low renin low aldo high K( RTA type 4)

  • Other types of renal disease with NSAID-

  • 1. allergic interstitial nephritis: within 3-10 days

  • 2. minimal change glomerulopathy- weeks after starting tx- presents with nephrotic range proteinuria


  • 1. 65 year old with H/o HTN, ventricular arrythmias controlled on Amiodarone, OA on NSAIds presents with puffiness on face on waking up. Has bilateral pitting dema. UA 3+ prot, 3 RBC., 15-20 WBC

  • 24 h prot – 4 g/day

  • BUN/creat 80/5

  • Serum albumin 2.8, TSH normal. The most likely diagnosis?

  • A) amiodarone induced hypothyroidism

  • B) RPGN

  • C) NSAIDs induced nephrotic sdr and interstitial nephritis


  • NSAIDs can cause all the following except:

  • 1) prerenal azotemia

  • 2) acute interstitial nephritis

  • 3) chronic interstitial nephritis

  • 4) nephrotic sdr

  • 5) ATN

  • 6) type 4 RTA


  • 1. Pregnant lady 18 w gestation, hardly gains any weight. C/o persistent nausea, vomiting for the past month. Creatinine increases from 0.5 to 1.9 DG?

  • 2. 60 year old patient presents with cellulitis of the leg. She is started on Clindamycin and PCN and patient defervesces in 24h. 5 days later, cellulitis is much improvd and patient has sudden onset of fever and a maculopapular rash with itching. You stop the drug. She has no dysuria or Foley’s catheter. What will you do next?

  • UA and Hansel Wright stain for eosinophils

  • Change antibiotics to cephalosporin


  • The UA shows 10 WBC, 7 RBC, Eosinophils +, casts negative. What is the most likely diagnosis?

  • A) nosocomial UTI

  • B) PCN induced interstitial nephritis

  • C) clindamycin induced nephrotoxicity

  • 2. All the following can cause interstitial nephritis except: A)antibiotics- PCN, cephalosporins, rifampin, Cipro, Sulfa

  • B) NSAIDs

  • C) diuretics( thiazide, furosemide)

  • D) dilantin

  • E) ACE inhibitors

Bactrim 4 renal effects
Bactrim 4 renal effects

  • 1. Sulfonamides induce renal failure by triggering allergic interstitial nephritis

  • 2. in high doses, Bactrim interferes with the renal secretion of potassium, resulting in hyperkalemia as in patients with PCP treated with Bactrim

  • 3. Bactrim competes for tubular secretion with creatinine and cause an increase in serum creatinine level

  • 4. long acting sulfonamides cause renal insuff by the crystals of the acetyl metabolite

Interstitial nephritis
Interstitial nephritis

  • Acute allergic IN

  • Chronic tubulointerstitial nephritis( analgesic nephropathy)

  • Acute allergic IN- presents with fever, maculopapular rash, eosinophilia with use of certain drugs or systemic inf

  • UA_ microscopic hematuria, pyuria, non nephrotic proteinuria, eosinophils+

  • Usually resolves after d/c of offending drug and steroids