Acute/allergic interstitial nephritis

- Maculopapular rash, fever, and new drug exposure (penicillin, tmp-smx, cephalosporins
nsaids, rifampin)
- AKI, pyuria, hematuria, wbc casts, eosinophilia, renal biopsy with inflammatory infiltrate
- Tx d/c drug and start GC if needed
- can sometimes be caused by infectious agents

chronic use can lead to CKD via chronic tubulointerstitial nephritis and papillary necrosis

Lower urinary tract sx – urgency, hesitancy, nocturia, weak stream with BPH do U/A and PSA to
assess for risk of prostate CA. Elevated Cr would show bilateral obstruction due to severe
bladder outlet obstruction and these pts require a renal u/s to assess for hydrophrosis and
exclude other causes of obstruction. A urinary catheter can provide quick relief.
Acyclovir has low urine solubility and the kidney rapidly excretes it. So it precipitates in the
renal rubles causing intratubular obstruction and direct renal tubular toxicity. It is most
common with IV acyclovir.
Adequate hydration and dosage adjustment with slow rate of infusion can help.

Aminoglycosides can be used in renal dysfunction but you must monitor serum levels and renal
function because they are nephrotoxic.

No screening for bladder CA b/c low incidence and poor testing

Gross painless hematuria
1. Bladder ca
2. Inf.
3. Trauma
4. Nephrolithiasis
5. Glomerulonephritis
6. Prostatic disease
Ddx. Start with U/a and r/o uti and confirm microhematuria and not myoglobinuria or
rifampin/beet ingestion.
Occupational hx – chemicals dyes
Drug exposure – cyclophosphamide or Smoking
Do contrast CT and cystoscopy to evaluate bladder and urethra
Abnormal hemostatis commonly seen in pt with CKD
- Abnormal bleeding and bruising (uremic coagulopathy)
- Now we only see ecchymoses and epistaxis b/c dialysis
- Guanidinosuccinic acid – uremic toxin normal pt/ptt platelets but increased bleeding
time and platlet dysfunction
- Tx desmopressin, cryoprecipitate and conjugated estrogen
End stage renal disease
- Dialysis OR Renal transplant

CV disease is the most common cause of death in dialysis and renal transplant patients

Contrast  Acute renal failure aka contrast induced nephropathy

- Renal vasocontriction and tubular injury
- Tx. Adequate hydration (isotonic bicarb or saline) or giving acetylcysteine (vasodilation
and antioxidant effects)

CO2 retention because of COPD can lead to CO2 narcosis (paco2 > 60) and acute hypercarbia
can be differentiated from chronic CO2 retention by associated acidosis and low bicarb. Chronic
CO2 retention will have high bicarb and normal pH.
industrial exposure (metal extraction in mining), niropursside, combustion of wool/silk
CN binds cytochrome oxidase and inhibits mitochondrial oxidative phosphorylation and cells
start glycolysis for ATP leading to lactic acidosis.
Tx. Na+ thiosulfate

if hypovolemic hypernatremic
- Step 1: restore volume with isotonic fluids
- Once euvolemic, start hypotonic fluid (5% dextrose is preferred over .45% saline)
- Correct Na by .5mEq/L/hr but not more than 12mEq/L/24hr
Do hemodialysis if lithium > 4 or >2.5 with significant toxicity (seizure, depressed mental status)

Screening for nephropathy in diabetics

Spot urine collection and timed urine collection for measurement of urine microalbumin to cr.
Ratio are good screening methods for microalbuminuria although 24 hr urine collection is most
accurate.