NP34 Nephrology

Acute Kidney Injury/Chronic Kidney Disease

Essential Med Notes 2015

adjust dosages of medications cleared by kidney (e.g. amiodarone, digoxin, cyclosporin,

tacrolimus, some antibiotics, and chemotherapeutic agents)
dialysis
3. definitive therapy depends on etiology
note: renal transplant is not a therapy for AKI
Prognosis
high morbidity and mortality in patients with sustained AKI and multi-organ failure

Chronic Kidney Disease

Definition
progressive and irreversible loss of kidney function
abnormal markers (Cr, urea)
GFR <60 mL/min for >3 mo; or
kidney pathology seen on biopsy; or
decreased renal size on U/S (kidneys <9 cm)
clinical features of CKD
volume overload and HTN
electrolyte and acid-base balance disorders (e.g. metabolic acidosis)
uremia

Incidence of Etiologies of CKD

DM
HTN
Glomerulonephritis
Other/Unknown
Interstitial nephritis/
Pyelonephritis
Cystic/Hereditary/Congenital
Secondary GN/Vasculitis

42.9%
26.4%
9.9%
7.7%
4.0%
3.1%
2.4%

Table 13. Stages of CKD (KDIGO, 2013)

Persistent Albuminuria Categories
A1
<30 mg/g
<3 mg/mEq

A2
30-300 mg/g
3-30 mg/mEq

A3
>300 mg/g
>30 mg/mEq

90

1 if CKD

G2

60-89

1 if CKD

G3a

45-59

G3b

30-44

G4

15-29

4+

G5

<15 (kidney failure)

4+

4+

4+

GFR (mL/
min/1.73m2)
G1
GFR categories
(mL/min/1.73m)

The numbers in the boxes are a reflection of the risk of progression and are a guide to the frequency of monitoring/year
"D" is added to G5 for patients requiring dialysis
Classification is based on cause, GFR, and amount of albuminuria
Rate of progression and risk of complications are determined by the cause of CKD

Management of Chronic Kidney Disease

diet
preventing HTN and volume overload
Na+ and water restriction
preventing electrolyte imbalances
K+ restriction (40 mEq/d)
PO43- restriction (1 g/d)
avoid extra-dietary Mg2+ (e.g. antacids)
preventing uremia and potentially delaying decline in GFR
protein restriction with adequate caloric intake in order to limit endogenous protein
catabolism
medical
adjust dosages of renally excreted medications
HTN: ACEI (target 130/80 or less), loop diuretics when GFR <25 mL/min
dyslipidemia: statins
calcium and phosphate disorders:
calcium supplements (e.g. TUMS) treats hypocalcemia when given between meals and
binds phosphate when given with meals
consider calcitriol (1,25-dihydroxy-vitamin D) if hypocalcemic
sevelamer (phosphate binder) if both hypercalcemic and hyperphosphatemic
vitamin D analogues are being introduced in the near future
cinacalcet for hyperparathyroidism (sensitizes parathyroid to Ca2+, decreasing PTH)
metabolic acidosis: sodium bicarbonate
anemia: erythropoietin injections (Hct <30%); target Hct 33-36%
clotting abnormalities: DDAVP if patient has clinical bleeding or invasive procedures (acts to
reverse platelet dysfunction)
dialysis (hemodialysis, peritoneal dialysis)
renal transplantation

Management of Complications of CKD

NEPHRON
N Low-nitrogen diet
E Electrolytes: monitor K+
P pH: metabolic acidosis
H HTN
R RBCs: manage anemia with
erythropoietin
O Osteodystrophy: give calcium
between meals (to increase Ca2+)
and calcium with meals (to bind
and decrease PO43-)
N Nephrotoxins: avoid nephrotoxic
drugs (ASA, gentamicin) and
adjust doses of renally excreted
medications

Renin Angiotensin System Blockade and

Cardiovascular Outcomes in Patients with
Chronic Kidney Disease and Proteinuria: A
Meta-Analysis
Am Heart J 2008;155:791-805
Purpose: To evaluate the role of RAS blockade in
improving cardiovascular CV outcomes in patients
with CKD.
Study Selection: Randomized controlled trials
that analyzed CV outcomes in patients with CKD/
proteinuria treated with RAS blockade (ACEI/ARB).
RAS blockade-based therapy was compared with
placebo and control therapy (-blocker, calciumchannel blockers, and other antihypertensive-based
therapy) in the study.
Results: Twenty-five trials (n=45,758) were
included. Compared to placebo, RAS blockade
reduced the risk of heart failure in patients with
diabetic nephropathy. In patients with non-diabetic
CKD, RAS blockade decreased CV outcome
compared to control therapy.
Conclusions: RAS blockade reduced CV outcomes
in diabetic nephropathy as well as non-diabetic CKD.