Remediation

Question 1

What are S/S of nephrititis (AGN)? Labs? Nature of the urine?

Answer 1

Sudden Edema – proteinuria, inability to excrete/regulate fluid balance
Aldosterone secretion
Decreased UOP
HTN
Cause: antigen-antibody complex causing inflammation of glomerulus and basement membrane  leaky basement membrane (to ALL things)

LABS:
BUN/Cr elevated
GFR/CrCl decreased
Hyperkalemia
Acidosis

Urine:
Dark, “cola-colored” urine
“Oliguria” = <400 mL UOP/24 hours
Proteinuria
Hematuria
Casts (clumps of RBC’s, WBC, proteins)

Question 2

What are S/S of nephrotic syndrome? Labs? Urine?

Answer 2

Definition: ** Proteinuria > 3.5 G/dL per 24 hours in URINE
24 hour urine test
Smaller tears in the glomerulus so rarer for RBC and WBC to get through.
Protein loss is not stopped so most s/s are caused by hypoalbuminemia
Cause: glomerular damage causes increased permeability of the glomerulus (selectively to PROTEINS)

S/S:
Hypoalbuminemia  decreased serum albumin, EDEMA (periorbital, extremities)
Hyperlipidemia  Hepatic compensation  creation of more proteins, but also more FATS (** Hyperlipidemia)
NOT inflammatory (contrasted from glomerulonephritis)
“leaky” blood vessels (decreased oncotic pressure)  Aldosterone release
Activation of RAAS, reabsorption of Na and H2O from kidneys, worsening edema and hypertension
“Foamy” urine

Question 3

What is AKI? LAbs? What is the nature of pre, intra and post?

Answer 3

AKI = sudden and (usually) reversible decline in renal function

decreased UOP,
BUN/Cr increased,
decreased GFR/CrCl,
Azotemia (increased BUN)

Pre-renal: anything that causes DECREASED perfusion to the kidneys
Hypovolemia: dehydration, hemorrhage
Hypotension: sepsis, trauma, CV disorders (MI, arrhythmia, CHF)
BUN/Cr ratio: > 20:1

Intra-renal (Intrinsic): Direct injury to the kidney (usually the nephron) causing acute tubular necrosis
ATN = damage to the filtering cells of the kidney. Necrotic cells slough off and obstruct tubules  unable to filter or excrete urine.
Causes = nephrotoxic medications, blood reaction, NSAIDS, IV contrast, GLOMERULONEPHRITIS

Post-renal: OBSTRUCTION. Typically caused by BPH, renal tones, cancer
Tx: Removal of obstruction
Complication: Hydronephrosis  dilation of ureter, renal pelvis and calyses
Increased glomerular pressure, decreased filtration, decreased GFR

Question 4

What is the oliguric, diuretis and recovery phases of AKI recovery?

Answer 4

Oliguric Phase (UOP < 400 mL/day)
Onset: hours/days after the injury
UA: Casts present
Increased BUN/Cr, K+
Uremia - increased BUN and Cr
Edema (pulmonary congestion, extremity, periorbital)
Neuro s/s
n/v, lethargy, fatigue, HA, reflex irritability, seizures, somnolence, coma, and death

Diuretic Phase (high UOP up to 5 L/day)
Lasts 1-2 weeks
Gradual increase in UOP
Hypovolemia and hypotension (due to fluid shifts)
Serum Cr and BUN remain high (Nephrons still not working)
Collecting duct cannot concentrate urine

Recovery Phase (repair of tissue, UOP 1-2 L/day)
BUN and Creatinine are normal

Question 5

What is chronic renal disease?

Answer 5

Gradual, progressive and irreversible
End organ damage to nephrons
Most common causes: Diabetes, Hypertension, long term nephrotoxic med use
Hypertension - constriction of renal blood vessels over time
DM (poorly controlled) – damage to glomeruli due to increased glucose levels, leading to proteinuria, glucosuria