NURS 5461 Renal 2 NEW EXAM 100% Verified
Prerenal ANSWER Caused by decreased perfusion to the kidneys. ▪ Etiologies include:
• GI bleeds, poor oral intake, diarrhea, vomiting • Diuretic, hyperglycemia, diabetes
insipidus8 • Fluids losses through the skin: diaphoresis, fever, burns • Heart Failure,
cirrhosis, nephrotic syndrome • Sepsis and septic shock, cardiogenic shock, any other
shock state • Renal artery stenosis • Hepatorenal syndrome • ACE inhibitors, ARBS,
direct renin inhibitors • NSAIDS • Calcineurin inhibitors
Evaluation PRE RENAL - ANSWER • CBC, BMP, Renal US, UA, FeNa, FEurea if they have
been receiving loop or thiazide diuretics
Treatment pre renal - ANSWER Treat the underlying cause, IV fluid replacement
It would be appropriate to give 1L of NS while you are working up the AKI and
determining the cause. If 1L of fluid improved the creatinine it is pre-renal. If the
creatinine is not improved by the 1L do not give any additional fluid until you have
diagnostic test results.
Intra-Renal - ANSWER Acute Tubular Necrosis • ATN results from ischemic or toxic
injury to the renal tubules. Epithelial cells in the 9 tubules become damaged, necrotic,
slough off and occlude the lumen of the tubules.
Causes - ANSWER o Ischemic injury ▪ Progression of pre-renal failure o
Mediations-Aminoglycosides, fluoroquinolones, vancomycin, acyclovir, tenofovir,
amphotericin, NSAIDS, ACE Inhibitors, ARBs, Calcineurin inhibitors
Clinical Presentation intra renal - ANSWER o Worsening renal function with the
appropriate history. o The creatinine will rise and at some point it will peak. It may go
very high. Once it peaks, it will begin to come down and return to baseline. Takes 1-3
weeks to resolve completely. o Once it begins to resolve the individual may experience a
diuresis, which needs to be monitored and fluid replaced accordingly
, Intrarenal Diagnosis - ANSWER o BUN:Creatinine ratio normal o UA- shows muddy
brown granular casts and epithelial cell casts o High urine sodium concentration > 40
mEq/L o FeNa > 2%, urine osmolality < 350
Treatment intrarenal - ANSWER o If it is related to a medication, stop the medication. o
Avoid nephrotoxins, electrolytes-treat abnormalities o **Do not give IV fluids. exception,
if they are not eating or drinking you may need to give maintenance fluids but monitor
them closely. Diuretics do not help with an ATN. Use only if the patient is experiencing
volume overload
Contrast Induced Nephropathy - ANSWER Persons at Greatest Risk o Those with a GFR
< 60ml/min o Diabetes Mellitus o Poor renal perfusion from Heart failure, dehydration or
liver disease (cirrhosis, liver failure) o High doses of contrast agent and those receiving
lowosmolar or high osmolar contrast
Clinical Picture CIN - ANSWER o Acute rise of creatinine 24 to 48 hours o Creatinine will
peak in 7 days and return to baseline in 10 days o Renal failure is usually reversible
unless baseline renal function is poor o Diagnosis is based on history of exposure
Treatment - ANSWER monitor electrolytes and treat abnormalities o Maintain renal
perfusion with IV hydration but monitor for volume overload o Avoid repeat contrast
exposure
Prevention is best CIN - ANSWER IV hydration with normal saline of sodium chloride
before and after the contrast study in high risk patients ▪ N-acetylcysteine (600mg to
1200mg PO BID) on the day before the study and on the day of the study. Research is
mixed on outcomes and potential benefits.
Acute Interstitial Nephritis - ANSWER Results from the infiltration of the renal interstitial
space by inflammatory cells. It is most commonly induced by drug therapy. o Most
common are PCN and cephalosporins
Clinical Presentation AIN - ANSWER Pts may present with vague symptoms of nausea,
vomiting, and malaise. Most are asymptomatic.
Prerenal ANSWER Caused by decreased perfusion to the kidneys. ▪ Etiologies include:
• GI bleeds, poor oral intake, diarrhea, vomiting • Diuretic, hyperglycemia, diabetes
insipidus8 • Fluids losses through the skin: diaphoresis, fever, burns • Heart Failure,
cirrhosis, nephrotic syndrome • Sepsis and septic shock, cardiogenic shock, any other
shock state • Renal artery stenosis • Hepatorenal syndrome • ACE inhibitors, ARBS,
direct renin inhibitors • NSAIDS • Calcineurin inhibitors
Evaluation PRE RENAL - ANSWER • CBC, BMP, Renal US, UA, FeNa, FEurea if they have
been receiving loop or thiazide diuretics
Treatment pre renal - ANSWER Treat the underlying cause, IV fluid replacement
It would be appropriate to give 1L of NS while you are working up the AKI and
determining the cause. If 1L of fluid improved the creatinine it is pre-renal. If the
creatinine is not improved by the 1L do not give any additional fluid until you have
diagnostic test results.
Intra-Renal - ANSWER Acute Tubular Necrosis • ATN results from ischemic or toxic
injury to the renal tubules. Epithelial cells in the 9 tubules become damaged, necrotic,
slough off and occlude the lumen of the tubules.
Causes - ANSWER o Ischemic injury ▪ Progression of pre-renal failure o
Mediations-Aminoglycosides, fluoroquinolones, vancomycin, acyclovir, tenofovir,
amphotericin, NSAIDS, ACE Inhibitors, ARBs, Calcineurin inhibitors
Clinical Presentation intra renal - ANSWER o Worsening renal function with the
appropriate history. o The creatinine will rise and at some point it will peak. It may go
very high. Once it peaks, it will begin to come down and return to baseline. Takes 1-3
weeks to resolve completely. o Once it begins to resolve the individual may experience a
diuresis, which needs to be monitored and fluid replaced accordingly
, Intrarenal Diagnosis - ANSWER o BUN:Creatinine ratio normal o UA- shows muddy
brown granular casts and epithelial cell casts o High urine sodium concentration > 40
mEq/L o FeNa > 2%, urine osmolality < 350
Treatment intrarenal - ANSWER o If it is related to a medication, stop the medication. o
Avoid nephrotoxins, electrolytes-treat abnormalities o **Do not give IV fluids. exception,
if they are not eating or drinking you may need to give maintenance fluids but monitor
them closely. Diuretics do not help with an ATN. Use only if the patient is experiencing
volume overload
Contrast Induced Nephropathy - ANSWER Persons at Greatest Risk o Those with a GFR
< 60ml/min o Diabetes Mellitus o Poor renal perfusion from Heart failure, dehydration or
liver disease (cirrhosis, liver failure) o High doses of contrast agent and those receiving
lowosmolar or high osmolar contrast
Clinical Picture CIN - ANSWER o Acute rise of creatinine 24 to 48 hours o Creatinine will
peak in 7 days and return to baseline in 10 days o Renal failure is usually reversible
unless baseline renal function is poor o Diagnosis is based on history of exposure
Treatment - ANSWER monitor electrolytes and treat abnormalities o Maintain renal
perfusion with IV hydration but monitor for volume overload o Avoid repeat contrast
exposure
Prevention is best CIN - ANSWER IV hydration with normal saline of sodium chloride
before and after the contrast study in high risk patients ▪ N-acetylcysteine (600mg to
1200mg PO BID) on the day before the study and on the day of the study. Research is
mixed on outcomes and potential benefits.
Acute Interstitial Nephritis - ANSWER Results from the infiltration of the renal interstitial
space by inflammatory cells. It is most commonly induced by drug therapy. o Most
common are PCN and cephalosporins
Clinical Presentation AIN - ANSWER Pts may present with vague symptoms of nausea,
vomiting, and malaise. Most are asymptomatic.
