NEPHROLOGY

Normal range in ABG

When does Kussmaul breathing occur

Metabolic acidosis

• Decreased HCO3 » Body compensates and tries to decrease pH by decreasing CO2 » increase RR

When must anion gap be computed

Metabolic Acidosis

• measured to find out what is causing acid buildup

• Differentiate between high and normal anion gap

Formula for Anion Gap

Normal: 8-12 mEqs/L

High": >12mEqs/L

• consider presence of organic acids that would cause increase in the anion gap

Causes of Normal vs High Anion Gap

Three Disorders of Renal Tubular Acidosis

RTA is NAGMA type of metabolic acidosis

Normal plasma K+

What level is considered severe hyperkalemia

Where is K+ excreted

N: 3.5-5.5 mM

Severe: >6 mM

90% urine 10% stool

4 Mechanisms that can cause hyperkalemia

1. Decrease in renal K+ excretion (due to decrease in aldosterone)

   • RAAS inhibitors (Inhibition of ACE and Angiotensin II pathway » decrease in aldosterone)

   • Hypoaldosteronism

   • Adrenal insufficiency (Addison disease)

2. Redistribution and reduced tissue uptake (beta blocker)

3. Excessive potassium intake (only if with renal failure)

4. Increase potassium release from tissues (tumor lysis syndrome, rhabdomyolysis)

Describe ECG changes based on K+ level

Treatment of hyperkalemia

7 Etiologies of hypokalemia

ECG change in hypokalemia

U waves

Bartter Syndrome vs Gitelman Syndrome

Clinical manifestations of hypercalcemia

Treatment of hypercalcemia

Clinical presentation of hypocalcemia

Treatment for hypocalcemia

Define the ff:

1. Anuria

2. Oliguria

3. Polyuria

Define AKI (3)

3 Classifications of AKI

Prerenal:

• Congestive Heart Failure

• Liver Failure

• Impaired renal autoregulation (NSAIDs ACE-I, ARBs)

Intrinsic:

• Glomerular - Acute Glomerulonephritis

• Tubules and Interstitium - ischemia, sepsis, infection, nephrotoxins

• Vascular - vasculitis, malignant, TTP-HUS

Postrenal:

• Obstructive

Most common intrinsic cause of AKI

Acute Tubular Necrosis

Urinalysis finding in Acute Tubular Necrosis

Muddy brown casts

Electrolyte profile of AKI - 5

1. Hyponatremia

2. Hyperkalemia, hypermagnesemia

3. Hyperphosphatemia

4. Hypocalcemia

5. Hyperuricemia

Peak GFR

120ml/min/1.73m2

Rate of decline of GFR by age

At the beginning of the third decade of life (20s), there is a normal annual decline in GFR by 1ml/min/1.73m2, GFR at age of 70 is at 70ml/min.1.73 (in a normal patient with comorbidities)

Define CKD

5 Etiologies of CKD

What determines CKD prognosis

1. GFR

2. Albuminuria (the higher the albuminuria >300mg/g the worse the prognosis)

When to use Cystatin C for eGFRcr

What CKD stage do complications (laboratory) usually appear

CKD Stage 3 and 4

Stages in CKD when gadolinium use should be limited/avoided:

• May cause nephrogenic systemic fibrosis (resembles skin changes seen in scleroderma)

CKD stage where anemia is universally present

Stage 4

CKD stage where peripheral neuropathy becomes clinically evident

Stage 4

5 clinical features of CKD

Indications for dialysis

AKI vs CKD in terms of:

1. Duration

2. History

3. Diagnostic Finding

4. Imaging

Lab Features of CKD (5)

Prevalence of nephrolith types 5

Most clinically important inhibitor of calcium containing stones

Urine citrate

Risk of stone doubles in what amount of urine per day

<1L urine per day

Vit C intake among males can increase the risk for

Calcium oxalate stones

• Vit C increases endogenous oxalic acid formation

Supplemental calcium intake increases risk for

1. calcium oxalate stone

2. calcium phosphate stone

Gold standard diagnostic test for nephrolithiasis

Helical CT scan without contrast

Treatment of nephrolith

medical expulsion therapy - tamsulosin 0.5mg OD PO, for distal nephrolith <6mm