NP28 Nephrology

Parenchymal Kidney/Systemic Disease with Renal Manifestation

Essential Med Notes 2015

Analgesic Nephropathies
1. Vasomotor AKI
normally prostaglandins vasodilate afferent renal arteriole to maintain blood flow
NSAIDs act by blocking cyclooxygenase enzyme, thereby preventing prostaglandin synthesis
and causing renal ischemia
more common in elderly, underlying renal disease, hypovolemia (diuretics, CHF, cirrhosis,
nephrotic syndrome)
clinically: develop prerenal azotemia within a few days of starting NSAID
treatment: discontinue NSAID, dialysis rarely needed
2. Acute Interstitial Nephritis
fenoprofen (60%), ibuprofen, naproxen
may be associated with minimal change glomerulopathy and nephrotic range proteinuria
resolves eventually with discontinuation of NSAID, may require interval dialysis
short-term high dose steroids (1 mg/kg/d of prednisone) may hasten recovery
3. Chronic Interstitial Nephritis
due to excessive consumption of antipyretics (phenacetin or acetaminophen) in combination
with NSAIDs
seen in patients who also have emotional stress, psychiatric symptoms, and GI disturbance
papillary necrosis
gross hematuria, flank pain, declining renal function
calyceal filling defect seen with IVP ring sign
increased risk of transitional cell carcinoma of renal pelvis
good prognosis if discontinue analgesics
4. Acute Tubular Necrosis
can be caused by acetaminophen
incidence of renal dysfunction is related to the severity of acetaminophen ingestion
vascular endothelial damage can also occur
both direct toxicity and ischemia contribute to the tubular damage
renal function spontaneously returns to baseline within 1-4 wk
dialysis may be required during the acute episode of ingestion
5. Other Effects of NSAIDs
sodium retention (2 to reduced GFR)
hyperkalemia, HTN (2 to hyporeninemic hypoaldosteronism)
excess water retention (due to elimination of ADH antagonistic effect of prostaglandins)

Systemic Disease with Renal Manifestation

Diabetes
diabetic nephropathy: presence of microalbuminuria or overt nephropathy (e.g. macroalbuminuria)
in patients with DM who lack indicators of other renal diseases
most common cause of end-stage renal failure in North America
35-50% of patients with type 1 DM will develop nephropathy, unknown percentage of type 2
at diagnosis up to 30% of patients with type 2 DM have albuminuria (75% microalbuminuria,
25% overt nephropathy)
microalbuminuria is a risk factor for progression to overt nephropathy and cardiovascular
disease
once macroalbuminuria is established, renal function declines, 50% patients reach ESRD within
7-10 yr
associated with HTN and diabetic retinopathy (especially type 1 DM) and/or neuropathy
(especially type 2 DM)
indication of possible non-diabetic cause of renal disease in patients with DM:
rising Cr with little/no proteinuria
lack of retinopathy or neuropathy (microvascular complications)
persistent hematuria (microscopic or macroscopic)
signs or symptoms of systemic disease
inappropriate time course; rapidly rising Cr, renal disease in a patient with short duration of DM
family history of non-diabetic renal disease (e.g. PCKD, Alports)

DM is one of the causes of ESRD that

does not result in small kidneys at
presentation of ESRD. The others are
amyloidosis, HIV nephropathy, PCKD,
and multiple myeloma

ACEI can cause hyperkalemia.

Therefore, be sure to watch serum K+,
especially if patient has DM and renal
insufficiency