Renal System

Question 1

Hematuria Gen Info

Answer 1

Defined as >3 erythrocytes/HPF on UA
microscopic hematuria mc glomerular in origin
gross hematuria mc nonglomerular or urologic in origin
Gross painless hematuria think bladder or kidney cancer until proven otherwise
May lead to obstruction if large clots form in the lower GU tract (potentially requiring bladder catheterization and irrigation)

Question 2

Hematuria causes

Answer 2

Intrarenal
- Tumor (RCC), infection (pyelo, abscess), stones, trauma
- glomerular disease, immunoglobulin A nephropathy
- strenuous exercise (marathon running), fever - benign
- polycystic kidney disease, simple cysts
- sickle cell disease
- analgesic nephropathy (renal papillary necrosis and chronic interstitial nephritis)
- renal papillary necrosis
Ureter
- tumor, infection (pyelo), stones, trauma
- stricture
Lower urinary tract (bladder, urethra, prostate)
- tumor (bladder, prostate), infection, stones, trauma (foley, invasive procedures)
- BPH - rarely
- chronic irritation
Other
- systemic diseases (SLE, rheumatic fever, HSP, granulomatosis with polyangiitis, HUS, goodpasture syndrome, PAN)
- bleeding disorders (hemophilia, thrombocytopenia)
- medications (cyclophosphamide, ACs, salicylates, sulfonamides)

Question 3

Hematuria diagnosis

Answer 3

urine dipstick
UA
microscopic > glomerular disease
gross > post-renal causes (trauma, stones, malignancy)
Infection > can cause either presentation
Examine urine sediment
- RBC casts + proteinuria > usually always GN
- pyuria > urine culture
+ dipstick but negative UA (no RBCs) > hemoglobinuria or - myoglobinuria (rhabdo)
Urine specimen for cytology; if suss high do cystoscopy regardless of cytology results (esp > 40y)
24 hr urine test for Cr and protein to assess renal function; also if +proteinuria
blood tests - coags, CBC, BUN/Cr
IVP, CT scan, US > if no cause found in above tests > look for stones, tumors, cysts, ureteral strictures, vascular malformations
Renal biosy > if suss glomerular disease

Question 4

Hematuria treatment

Answer 4

treat underlying cause; maintain urine volume

Question 5

Proteinuria gen info

2 types and other causes

Answer 5

Urinary excretion of >150 mg protein/24 hours
Glomerular
* increased glomerular permeability to proteins from various causes
* Can lead to nephrotic syndrome
* May be seen in all types of GN
* Protein loss tends to be more severe than in nonglomerular causes
b. Tubular
* Small proteins normally filtered at the glomerulus then reabsorbed by the
tubules appear in the urine because of abnormal tubules (ie., due to derm
tubular reabsorption)
* Proteinuria and kidney damage tends to be less severe due to a lower quantity
and nephrotoxicity of the associated proteins
* Causes include sickle cell disease, urinary tract obstruction, and interstitial
nephritis
c. Overflow proteinuria-increased production of small proteins overwhelms the tubules’ ability to reabsorb them (e.g., Bence Jones protein in multiple myeloma,
myoglobin in rhabdomyolysis)
d. Other causes of proteinuria (all of the following can affect renal blood flow)
* UTI
* Fever, heavy exertion/stress, CHF
* Pregnancy
* Orthostatic proteinuria- occurs when the patient is standing but not when
recumbent; self-limited and benign

Question 6

Proteinuria - nephrotic syndrome key features

Answer 6

a. Key Features
• Urine protein excretion rate >3.5 g/24 hours
• Hypoalbuminemia- hepatic albumin synthesis cannot keep up with urinary protein losses = decreased plasma oncotic pressure > edema.
• Edema- often the initial complaint (pedal edema, periorbital, anasarca, ascites, pleural effusion). Increased
aldosterone secretion exacerbates the problem (increases sodium reabsorption).
• Hyperlipidemia and lipiduria- increased hepatic synthesis of LDL and VLDL
because liver is revving up albumin synthesis.
• Hypercoagulable state (due to loss of certain anticoagulants in the urine).
increased risk of thromboembolic events (deep venous thrombosis, pulmonary
embolism, renal vein thrombosis).
• Increased incidence of infection–results from loss of immunoglobulins in the
urine, particularly susceptible to pneumococcal infections.

Question 7

Proteinuria - nephrotic syndrome causes

Answer 7

b. Nephrotic syndrome usually indicates significant glomerular disease (either primary or secondary to systemic illness) as the underlying cause is abnormal glomerular permeability
Causes
• Primary glomerular disease (50% to 75% of cases)- membranous nephropathy mc in adults (40% of cases), then focal segmental glomerulosclerosis (FSGS) (35%) and membranoproliterative GN (15%). Minimal change disease (MCD) mc in children (75% of cases).
• Secondary glomerular pathology:
• Systemic disease–diabetes, collagen vascular disease, SLE, RA, Henoch-
Schönlein purpura, polyarteritis nodosa (PAN), granulomatosis with polyangiitis.
• Amyloidosis, cryoglobulinemia.
• Drugs/toxins- captopril, heroin, heavy metals, NSAIDs, penicillamine.
• Infection- bacterial, viral, protozoal.
• Multiple myeloma, malignant HTN, transplant rejection.

Question 8

Proteinuria Diagnosis

Answer 8

B. Diagnosis
1. Urine dipstick test (read color changes)
2. Urinalysis
a. Initial test once detected by dipstick test.
b. Examination of urine sediment is important.
• RBC casts suggest GN.
• WBC casts suggest pyelonephritis and interstitial nephritis.
• Fatty casts suggest nephrotic syndrome (lipiduria).
C. If urinalysis confirms the presence of protein, a 24-hour urine collection (for albumin and Cr) appropriate to establish the presence of significant proteinuria.
3. Test for microalbuminuria
a. albumin excretion 30-300 mg/day.
b. This is below the range of sensitivity of standard dipsticks. Special dipsticks can
detect microgram amounts of albumin. If test result is positive, do radioimmunoassay (most sensitive and specific test for microalbuminuria),
c. Microalbuminuria can be early sign of diabetic nephropathy; often presents before any other lab abnormality or overt sxs.
4. Other tests to determine etiology (may or may not be necessary depending on case)
a. Cr clearance- best test of renal function/GFR estimation
b. Serum BUN and Cr
c. CBC, vitamin D–to detect anemia due to renal failure
d. Serum albumin level–varies inversely with degree of proteinuria
e. Renal ultrasound–to detect obstruction, masses, cystic disease
f. Intravenous pyelogram (IVP)- to detect chronic pyelonephritis
g. Immunologic tests: ANA levels (lupus), antiglomerular basement membrane
(Goodpasture syndrome), hepatitis serology (causes of MN, MPGN), antistreptococcal antibody titers (PSGN), complement levels, cryoglobulin studies
h. Serum and urine electrophoresis (myeloma)
i. Renal biopsy–if no cause is identified by less invasive means

Question 9

Proteinuria Treatment

Answer 9

1. Asymptomatic proteinuria.
   a. If transient, no further workup or treatment is necessary.
   b. If persistent, further testing is indicated. Start by checking BP and examining
   urine sediment. Treat the underlying condition and associated problems (e.g
   hyperlipidemia).
2. Symptomatic proteinuria- further testing is always required.
   a. Treat the underlying disease (diabetes, multiple myeloma, SLE, MCD).
   b. ACE inhibitors (ARB cannot tolerate ACE) > decrease urinary albumin loss.
   They are an essential part of treatment for diabetics with HTN and should be
   started before fixed albuminuria is present.
   c. Diuretics- if edema present.
   d. Limit dietary protein and sodium.
   e. Treat hypercholesterolemia (using diet or a lipid-lowering agent)
   f. Anticoagulate if thrombosis occurs. Currently, there is not enough data to support routine prophylactic anticoagulation of these patients and must be considered on case-by-case basis.
   g. Vaccinate against influenza and pneumococcus–there is an increased risk of infection in these patients.

Question 10

AKI gen info

Answer 10

Rapid decline in renal function, with an increase in serum creatinine level (while the cutoff for rise in creatinine which qualifies as an “injury” is controversial, an increase as little as 0.3 mg/dL may have clinical relevance, while traditional definitions describe relative increase of 50% or absolute increase of 0.5 to 1.0 mg/dL). The creatinine may be normal despite a markedly reduced GFR in the early stages due to the time it takes for creatinine to accumulate in body. Also called acute renal failure (ARF).
2. One consensus definition- RIFLE criteria.
a. RISK: 1.5-fold increase in the serum creatinine or GFR decrease by 25% or urine output <0.5 mL/kg/hr for 6 hours.
b. INJURY: Two fold increase in the serum creatinine or GFR decrease by 50% or
urine output <0.5 mL/kg/hr for 12 hours.
c. FAILURE: Threefold increase in the serum creatinine or GFR decrease by 75% or urine output of <0.5 mL/kg/hr for 24 hours, or anuria for 12 hours.
d. LOSS: Complete loss of kidney function (i.e., requiring dialysis) for more than 4 weeks
e. ESRD: Complete loss of kidney function (i.e., requiring dialysis) for more than 3 months
3. AKI may be nonoliguric, oliguric, or anuric. Severe AKI may occur without a reduction in urine output (nonoliguric AKI).
a. General goals of therapy are reversing the initial insult to the kidney and/or supportive care as GFR recovers, as well as preventing fulminant kidney failure requiring temporary or permanent hemodialysis.
4. Weight gain and edema are mc sx. Due to positive water and sodium (Na*) balance.
5. Characterized by azotemia (elevated BUN and Cr).
a. Elevated BUN is also seen with catabolic drugs (e.g., steroids), GI/soft tissue bleeding (due to RBC digestion and reabsorption of urea), and dietary protein intake.
b. Elevated Cr is also seen with increased muscle breakdown and various drugs. The baseline Cr level varies proportionately with muscle mass.
6. Prognosis
a. More than 80% recover completely but
prognosis varies widely depending on AKI severity and other comorbidities.
b. MC cause of death is infection (75% of all deaths), followed by cardiorespiratory complications. Other complications include chronic kidney injury and need for dialysis

Prerenal azotemia and ischemic AKl are part of a spectrum of manifestations of renal hypoperfusion. The latter differs in that injury to renal tubular cells occurs.

Question 11

AKI categories - Prerenal failure causes

Answer 11

1. Prerenal failure
   a. MC cause of AKI; potentially reversible
   b. Etiology (decrease in systemic arterial blood volume or renal perfusion leading to
   renal ischemia) — can complicate any disease that causes hypovolemia, low cardiac
   output, or systemic vasodilation
   • Hypovolemia- dehydration, excessive diuretic use, poor fluid intake, vomiting, diarrhea, burns, hemorrhage
   • CHF, cardiorenal syndrome
   • Hypotension (SBP<90 mm Hg), from sepsis, excessive antihypertensive medications, bleeding, dehydration
   • Renal arterial obstruction (kidney is hypoperfused despite elevated blood pressure)
   • Cirrhosis, hepatorenal syndrome
   • In patients with decreased renal perfusion, NSAIDs (constrict afferent arteriole), ACE inhibitors (cause efferent arteriole vasodilation), and cyclosporin can precipitate prerenal failure.

Question 12

Monitoring a Patient With AKI

Answer 12

• Daily weights, intake, and output (worsening volume status can be an indication for urgent dialysis)
• BP
• Serum electrolytes (hyperkalemia and acidosis can also be indications for urgent dialysis, also tend toward hyponatremia and hyperphosphatemia)
• Hb and Het (for anemia)
• Watch for signs of infection

Question 13

Diagnostic Approach in AKl

Answer 13

• H&P
• First determine duration of renal failure by knowing the baseline Cr level
• Second determine whether AKI is due to prerenal, postrenal causes, intrarenal last. This is done via a combination of H&P and laboratory findings.
• Signs of volume depletion, CHF or cirrhosis suggest prerenal etiology.
• Signs of allergic reaction (rash) suggest acute interstitial nephritis (an intrinsic renal etiology)
• A suprapubic mass, BPH, or bladder dysfunction suggests postrenal etiology.
• Medication review
• Urinalysis
• Urine chemistry (FENa or FEUrea, osmolality, urine Na*, urine Cr, urine BUN)
• Renal US (r/o obstruction)

Question 14

Prerenal vs Intrinsic Renal quick hit

Answer 14

Prerenal
BUN/Cr Ratio >20:1
Urine osmolarity >500
Urine Na* <20
FENa < 1%
Urine sediment - scant; hyaline casts

Intrinsic Renal
BUN/Cr Ratio <20:1
Urine osmolarity > 250-300
Urine Na* > 40
FENa > 2-3%
Urine sediment - abnormal

ATN
Urine osmolarity > 350
Urine Na* > 40
FENa > 1%
Urine sediment - full brownish pigment, granular casts with epithelial casts

Question 15

AKI categories - Prerenal failure patho, sxs, dx

Answer 15

c. Pathophysiology
• Renal blood flow decreases enough to lower the GFR > decreased clearance of metabolites (BUN, Cr, uremic toxins).
• Because the renal parenchyma is undamaged, tubular function (and therefore the concentrating ability) is preserved > kidney responds appropriately, conserving as much sodium and water as possible.
• This form of AKI is reversible on restoration of blood flow; but if hypoperfusion persists, ischemia results and can lead to acute tubular necrosis (ATN)
d. Clinical features
• Signs of volume depletion (dry mucous membranes, hypotension, tachycardia, decreased tissue turgor, oliguria/anuria)
e. Lab findings
• Oliguria- always found in prerenal failure (this is to preserve volume)
• Increased BUN-to-serum Cr ratio (>20:1 is the classic ratio) because kidney can reabsorb urea to increase sodium and water retention
• Increased urine osmolality (>500 mOsm/kg H2O)- because the kidney is able to appropriately reabsorb water
• Decreased urine Na (<20 mEg/L with fractional excretion of sodium FENa<1%) because Na is avidly reabsorbed
• Increased urine-plasma Cr ratio (>40:1)- because much of the filtrate is reabsorbed (but not the creatinine).
• Bland urine sediment, indicating lack of significant cellular damage to glomeri or
tubules

Question 16

AKI categories - Intrinsic Renal Failure Causes

Answer 16

a. Kidney tissue (interstitium, glomeruli, tubules) is damaged such that glomerular filtration and tubular function are significantly impaired > kidneys unable to concentrate urine effectively.
b. Causes
• Tubular disease (ATN)- can be caused by ischemia MC, nephrotoxins
• Glomerular disease (acute glomerulonephritis (GN) ex Goodpasture syndrome, granulomatosis with polyangiitis, post-streptococcal GN, lupus
• Vascular disease- ex renal artery occlusion, TTP, HUS
• Interstitial disease- ex allergic interstitial nephritis, often due to a hypersensitivity reaction to medication

Question 17

Rhabdomyolysis

Answer 17

Skeletal muscle breakdown caused by trauma, crush injuries, prolonged immobility, seizures, snake bites
2. Release of muscle fiber contents (myoglobin) into bloodstream. Myoglobin is toxic to kidneys, which can lead to AKI via tubular damage and obstruction.
3. Presents with sequelae of cell death: markedly elevated creatine phoshokinase (CP%), hyperkalemia, hypocalcemia (due to released phosphate), hyperuricemia.
4. Treat with IV fluids, mannitol (osmotic diuretic) and bicarbonate (drives K back into cells).

Question 18

Causes of Acute Tubular Necrosis (ATN)

Answer 18

Ischemic AKI
• Secondary to severe decline in renal blood flow, as in shock, hemorrhage, sepsis, DIC, HF
• Ischemia results in the death of tubular cells
Nephrotoxic AKI
• Injury secondary to substances that directly injure renal parenchyma and result in cell death.
• causes include antibiotics (aminogiycosides, vancomycin), radiocontrast agents, NSAIDs especially in the setting of CHF), poisons, myoglobinuria (from muscle damage, rhabdomyolysis, strenuous exercise), hemoglobinuria (from hemolysis), chemotherapeutic drugs (cisplatin), kappa and gamma light chains
produced in multiple myeloma.

Question 19

Course of ATN

Answer 19

• Onset (insult)
• Oliguric phase
- Azotemia and uremia- average length 10 to 14 days
- Urine output
• Diuretic phase
- Begins when urine output is >500 mL/day
- High urine output due to the following: fluid overload (excretion of retained salt, water, other solutes that were retained during oliguric phase); osmotic diuresis due to retained solutes during oliguric phase; tubular cell damage (delayed recovery of epithelial cell function relative to GFR)
• Recovery phase- recovery of tubular function

Question 20

AKI categories - Intrinsic Renal Failure SXS, DX

Answer 20

c. Clinical features depend on the cause. Edema is usually present. Recovery may be
possible but takes longer than in prerenal failure.
d. Laboratory findings
• Decreased BUN-to-serum Cr ratio (<20:1, typically closer to 10:1 ratio) in com-
parison with prerenal failure. Both BUN and Cr levels are still elevated, but less
urea is reabsorbed than in prerenal failure as kidney is no longer actively reabsorbing it.
• Increased urine Na (>40 mEq/L with FENa > 2% to 3%) because Na is
poorly reabsorbed
• Decreased urine osmolality (<350 mOm/kg H,O) because renal water reabsorption is impaired
• Decreased urine-plasma Cr ratio (<20:1) because filtrate cannot be reabsorbed

Question 21

AKI categories - post renal failure causes, dx

Answer 21

a. Least common cause of AKI
b. Obstruction of any segment of the urinary tract (with intact kidney) causes
increased tubular pressure (urine produced cannot be excreted), which leads to
decreased GFR. Blood supply and renal parenchyma are intact. Note that both
kidneys must be obstructed (e.g., prostatic enlargement) for creatinine to rise.
c. Renal function is restored if obstruction is relieved before the kidneys are damaged.
d. Postrenal obstruction, if untreated, can lead to ATN.
e. Causes
• Urethral obstruction secondary to enlarged prostate (BPH) is the most common
cause
• Obstruction of solitary kidney
• Nephrolithiasis
• Obstructing neoplasm (bladder, cervix, prostate, and so on)
• Retroperitoneal fibrosis
• Ureteral obstruction is an uncommon cause bc obstruction must be bilateral to cause renal failure.

DX
PE - palpate bladder
US - look for obstruction, hydronephrosis
Catheter - look for large urine output

Question 22

AKI general diagnosis

8 diagnostics

Answer 22

1. Blood tests
   a. Elevation in BUN and Cr levels. Be aware that small changes in Cr may reflect a
   much more significant decrease in GFR.
   b. Electrolytes (retention of K, PO, drop in HCO3 indicating acidosis, decrease in
   Na due to fluid retention)
   c. Albumin levels to monitor for nephrotic syndrome
   d. CBC with differential
2. Urinalysis
   a. A dipstick test positive for protein (3+, 4+) suggests intrinsic renal failure due to
   glomerular insult.
   b. Microscopic examination of the urine sediment:
   * Crystals indicate presence of stones.
   * Micro-organisms are seen in both infection and nonpathogenic colonization
   (differentiation made based on symptoms).
   * Granular casts degeneration of cells and protein aggregates seen in ATN
   (“muddy brown” casts)
   * Hyaline casts are devoid of contents (seen in pre-renal failure).
   * RBC casts indicate glomerular disease.
   * WBC casts indicate renal parenchymal inflammation.
   * Fatty casts indicate nephrotic syndrome.
3. Urine chemistry–to distinguish between different forms of AKI.
   a. Urine Na, Cr, and osmolality: Urine Na depends on dietary intake.
   b. FENa: collect urine and plasma electrolytes simultaneously = [(UNa)/(PlasmaNa)/(UCr)/(Pir) x 100]
   * < 1% suggest prerenal failure.
   * > 2% to 3% suggest ATN.
   * FENa is most useful if oliguria is present.
   * If patient is on diuretics, UNa will be artificially elevated and fractional excretion
   of urea (FEUrea) must be used instead.
   c. Renal failure index 5 (uNa/[uCr/pCr]) × 100)
   * < 1% suggest prerenal failure.
   * > 1% suggest ATN.
4. Urine culture and sensitivities- if infection is suspected
5. Renal ultrasound.
   a. Primarily useful for evaluating kidney size and for excluding urinary tract
   obstruction (i.e., postrenal failure)- presence of bilateral hydronephrosis or
   hydroureter
   b. Order for most patients with AKI- unless the cause of the AKI is obvious and is
   not postrenal
6. CT scan AP- may be helpful in some cases; usually done if renal
   ultrasound shows an abnormality such as hydronephrosis
7. Renal biopsy- useful occasionally if there is suspicion of acute GN or acute allergic
   interstitial nephritis
8. Renal arteriography- to evaluate for possible renal artery occlusion; should be per-
   formed only if specific therapy will make a difference

Question 23

UA findings - Preprenal

Answer 23

Urine Sediment - benign; few hyaline casts
Protein - negative
Blood - negative

Question 24

UA findings - Intrarenal

Answer 24

ATN
Urine Sediment - “muddy brown” casts, renal tubular cells/casts, granular casts
Protein - trace
Blood - negative

AGN
Urine Sediment - dysmorphic RBCs, RBs with casts, WBCs
with casts, fatty casts
Protein - 4+
Blood - 3+

AIN
Urine Sediment - RBCs, WBCs, WBCs with casts, eosinophils
Protein - 1+
Blood - 2+

Question 25

AKI complications

Answer 25

1. ECF volume expansion and resulting pulmonary edema–treat with a diuretic (furosemide)
   In the early phase of AKI, the most common mortal complications are hyperkalemic cardiac arrest and pulmonary edema.
2. Metabolic
   a. Hyperkalemia- due to decreased excretion of K and the movement of potassium from ICF to ECF due to tissue destruction and acidosis
   b. Metabolic acidosis (with increased anion gap) due to decreased excretion of hydrogen ions; if severe (below 16 mEq/L), correct with sodium bicarbonate
   c. Hypocalcemia-loss of ability to form active vitamin D and rapid development of PTH resistance
   d. Hyponatremia may occur if water intake is greater than body losses, or if a volume depleted patient consumes excessive hypotonic solutions. (Hypernatremia may also be seen in hypovolemic states.)
   e. Hyperphosphatemia- due to decreased clearance
   f. Hyperuricemia
3. Uremia- toxic end products of metabolism accumulate (especially from protein metabolism), leading to;
   a. Platelet dysfunction
   b. Immune dysfunction
   c. Pericarditis
   d. Encephalopathy
4. Infection
   a. A common and serious complication of AKI (occurs in 50% to 60% of cases). Cause is probably multifactorial, but uremia itself is thought to impair immune function.
   b. Examples include pneumonia, UTI, wound infection, and sepsis.

Question 26

AKI treatment general measures

Answer 26

1. General measures
   a. Avoid medications that decrease renal blood flow (NSAIDs) and/or that are nephrotoxic (e.g., aminoglycosides, radiocontrast agents).
   b. Adjust medication dosages for level of renal function
   c. Correct fluid imbalance:
   • If volume depleted, give IV fluids. However, many patients with AKI are volume overloaded (especially if they are oliguric or anuric), so diuresis may be necessary.
   • Goal is to strike a balance between correcting volume deficits and avoiding volume overload (while maintaining adequate urine output). Remember that urine output is a reflection of renal blood flow (volume status) and GFR (kidney function).
   • Monitor fluid balance by daily weight measurements (most accurate estimate) and intake-output records.
   • Be sure to take into account the patient’s cardiac history when considering treatment options for fluid imbalances (i.e., do not give excessive fluid to a patient with CHF).
   d. Correct electrolyte disturbances if present.
   e. Optimize cardiac output. BP should be approximately 120-140/80-90.
   f. Order dialysis if symptomatic uremia, intractable acidemia, hyperkalemia, or volume overload develop. Indications for urgent dialysis often remembered by “AEIOU” mnemonic: Acidosis, Electrolytes, Intoxications (such as in overdoses),
   volume Overload, Uremia.

Question 27

Prognostic Factors in AKI

Answer 27

Severity of renal failure:
Magnitude of increase in Cr
Presence of oliguria
Fractional excretion of sodium
Requirement for dialysis
Duration of severe renal failure
Marked abnormalities on urinalysis
Underlying health of patient:
Age
Presence, severity, and reversibility of underlying disease
Clinical circumstances:
Cause of renal failure
Severity and reversibility of acute process(es)
Number and type of other failed organ systems
Development of sepsis and other complications

Question 28

AKI treatment Prerenal

Answer 28

2. Prerenal
   a. Treat the underlying disorder (such as hypovolemic or cardiogenic shock).
   b. Give fluids to maintain euvolemia and restore blood pressure–do not give to patients with edema or ascites. May be necessary to stop antihypertensive medications. Remember that NS is often preferred unless acidemia is present (may worsen
   with hyperchloremia), in which case LR can be used.
   c. Eliminate any offending agents (ACE inhibitors, NSAIDs).
   d. If patient is unstable, Swan-Ganz monitoring for accurate assessment of intravascular volume.

Question 29

AKI treatment Intrarenal

Answer 29

3. Intrinsic
   a. Once AT develops, therapy is supportive and renal function generally recovers. Eliminate the cause/offending agent.
   b. If oliguric, a trial of furosemide may help to increase urine flow. This improves fluid balance.

Question 30

AKI treatment Post renal

Answer 30

4. Postrenal- bladder catheter may be inserted to decompress the urinary tract. Consider urology consultation.
   a. Be aware of the potential for post-obstructive diuresis and a rapid increase in urine output when obstruction is resolved, which may require IV fluid replacement.

Question 31

Potassium metabolism

Answer 31

• Normal K levels: 3.5 to 5.0 mEgL.
• Location in the body- most of the body’s potassium (98%) is intracellular
• Hypokalemia- alkalosis and insulin administration may cause hypokalemia because they cause a shift of potassium into the cells
• Hyperkalemia- acidosis and anything resulting in cell lysis increase serum K (both force K out of cells into the ECF).
• Potassium secretion- most of the excretion of potassium occurs through the kidneys (80%); the remainder occurs via the Gl tract. Aldosterone plays an important role in renal potassium secretion.
Serum potassium is affected by pH: alkalosis > hypokalemia
acidosis > hyperkalemia
Check K levels in pt with CHF + taking diuretics + digoxin > may be hypokalemic > predisposes to digoxin toxicity

Question 32

Hypokalemia causes

Answer 32

1. Gl losses - normotensive
   a. Vomiting and nasogastric drainage (volume depletion and metabolic alkalosis also result)
   b. Diarrhea - common cause of both hypoK and NAGMA
   c. Laxatives and enemas
   d. Intestinal fistulas particularly after IBD
   e. Decreased potassium absorption in intestinal disorders
2. Renal losses - normotensive
   a. Diuretics
   b. Renal tubular or parenchymal disease
   c. Primary and secondary hyperaldosteronism - will have HTN
   d. Excessive glucocorticoids- due to mineralocorticoid action at high serum levels
   e. Magnesium deficiency
3. Bartter syndrome- chronic volume depletion secondary to an autosomal-recessive defect in salt reabsorption in the thick ascending limb of the loop of Henle > hyperplasia of juxtaglomerular apparatus > increased renin levels and secondary aldosterone elevations.
4. Other causes
   a. Insufficient dietary intake
   b. Insulin administration
   c. Certain antibiotics especially amphotericin B
   d. Profuse sweating
   e. Epinephrine (B2-agonists)- hypokalemia occurs in 50% to 60% of trauma patients, perhaps due to increased epinephrine levels

Question 33

Hypokalemia Clinical Features

Answer 33

1. Arrhythmias- prolongs normal cardiac conduction
   a. Exacerbates digitalis toxicity
   b. Flattening of T waves on EKG. U waves appear if severe
2. Muscular weakness, fatigue, paralysis, and muscle cramps
3. Decreased deep tendon reflexes
4. Paralytic ileus
5. Polyuria and polydipsia
6. Nausea/vomiting

Question 34

Hypokalemia Treatment

Answer 34

1. Identify and treat the underlying cause
2. Discontinue any medications that can aggravate hypokalemia.
3. Oral KCl is the preferred (safest) method of replacement and is appropriate in most instances. Always retest the K levels after administration.
   a. Using 10 mEq of KCI usually increases K levels by 0.1 mEq/L, it will increase levels more in patients with renal insufficiency due to decreased clearance.
   b. It comes in slow-acting and fast-acting forms.
4. IV KCI can be given if hypokalemia is severe (<2.5), if the patient cannot take PO or if the patient has arrhythmias secondary to hypokalemia.
   a. Give slowly to avoid hyperkalemia.
   b. Monitor K concentration and monitor cardiac rhythm when giving IV potssium
   c. Infusion pearls.
   • Maximum infusion rate of 10 mEq/hr in peripheral IV line.
   • Maximum infusion rate of 20 mEg/hr in central line.
   • May add 1% lidocaine to bag to decrease pain (potassium burns!)
   S. As with calcium, it is difficult to correct the potassium level if any hypomag is not corrected first.

Question 35

Hyperkalemia causes

Answer 35

1. Increased total-body potassium
   a. Renal failure (acute or chronic)
   b. Hypoaldosterone states: Addison disease, hyporeninemic hypoaldosteronism, ACE inhibitors, potassium-sparing diuretics (spironolactone)
   c. latrogenic-excessive doses of potassium (use caution when administering potassium in patients with renal failure) and certain medications (e.g., trimethoprim-sulfamethoxazole)
   d. Blood transfusion- usually due to lysed cells
2. Redistribution- translocation of potassium from intracellular to extracellular space
   a. Acidosis (notably not seen in lactic or ketoacidosis)
   b. Tissue/cell breakdown- thabdomyolysis (muscle breakdown), chemotherapy, hemolysis, burns
   c. Gl bleeding
   d. Insulin deficiency- insulin stimulates the NaK -ATPase and causes K to shift into cells. So insulin deficiency and hypertonicity (high glucose) promote K shifts from ICF to ECF
   e. Rapid administration of B-blocker
3. Pseudohyperkalemia (spurious)
   a. This refers to an artificially elevated plasma K concentration due to K movement out of cells immediately before or after venipuncture. Contributing factors include prolonged use of a tourniquet with or without repeated fist clenching. This
   can cause acidosis and subsequent K loss from cells leading to falsely elevated result. Test should be repeated.
   b. Additionally, if the sample is not processed quickly, some red blood cells will hemolyze and cause spillage of K > falsely elevated result > repeat test
   c. Other contributing factors include leukocytosis and thrombocytosis

Question 36

Hyperkalemia clinical features

Answer 36

Hyperkalemia inhibits renal ammonia synthesis and reabsorption. Thus, net acid excretion is impaired and results in metabolic acidosis further exacerbating hyperkalemia due to K*
movement out of cells.

B. Clinical Features
1. Arrhythmias- most important effect of hyperkalemia is on the heart. Check an ECG immediately in a hyperkalemic patient. With increasing potassium, ECG changes progress through tall, peaked T waves, QRS widening, PR interval prolongation, loss of P waves, and finally a sine-wave pattern.
2. Muscle weakness and (rarely) flaccid paralysis
3. Decreased deep tendon reflexes
4. Respiratory failure
5. Nausea/vomiting, intestinal colic, diarrhea
6. Acidosis due to decreased ammonium formation in renal tubules

Question 37

Hyperkalemia treatment

Answer 37

1. If the hyperkalemia is severe, or if ECG change is present, first give IV calcium.
   a. Calcium stabilizes the resting membrane potential of the myocardial membrane-
   aka decreases membrane excitability.
   b. Use caution in giving calcium to patients on digoxin (hypercalcemia predisposes to digoxin toxicity.)
2. Shift potassium into the intracellular compartment
   a. Glucose and insulin- works via stimulation of Na/K pump. Glucose alone will stimulate insulin from beta cells, but exogenous insulin is more rapid (and thus should be one of the first steps in management). Give both to prevent hypoglycemia.
   b. Beta agonists (e.g., albuterol)- also works via stimulation of Na/K pump. Transient
   management in those with symptoms or EKG changes.
   c. Sodium bicarbonate- increases pH level, which shifts K into cells via H+/K
   pump. Similar to B agonists, an emergency measure in severe hyperkalemia.
3. Remove potassium from the body.
   a. Kayexalate- Gl potassium exchange resin (Na/K exchange in Gl tract) absorbs
   K+ in the colon, preventing reabsorption (passed in stool, thus reliant on patient being able to defecate)
   b. Diuretics (furosemide)- effect is variable and thus is rarely used as monotherapy.
   c. Hemodialysis.
   • Most rapid and effective way of lowering plasma K
   • Reserved for intractable hyperkalemia (usually over 7) and for those with renal
   failure

Question 38

Nephrotic Syndrome gen info

Answer 38

Kidney disease: significant proteinuria, hypoalbuminemia, peripheral edema, and hyperlipidemia.
Defined as proteinuria > 3.5 g per 24 hours or spot urine protein to creatinine ratio > 3,000-3,500 mg/g (300-350 mg/mmol) plus hypoalbuminemia and edema
Common presentation: progressive lower extremity edema and fatigue.
Also periorbital edema (accentuated by periods of recumbency), hypertension, pleural and pericardial effusion, and frothy urine. Initial presentation can be thromboembolic event.
80%-90% caused by primary glomerular diseases (can also be primary or secondary) like focal segmental glomerulosclerosis, membranous nephropathy, or minimal change disease; secondary causes include diabetic nephropathy, lupus, plasma cell dyscrasias (amyloidosis, light or heavy chain deposition dz), and infections (HIV, parvovirus B19, CMV, EBV, hepatitis, syphilis), SCD, malignancy, toxins (NSAIDs, aminoglycosides, amphotericin, captopril, tamoxifen, pencillamine, lithium) Complications resulting from loss of low-molecular-weight proteins in the urine and overproduction of proteins in the liver.

Question 39

Nephritic syndrome gen info

Answer 39

Defined by presence of glomerular hematuria, sub-nephrotic range proteinuria, abnormal kidney function (such as azotemia), and hypertension.

Question 40

Nephrotic Syndrome patho

Answer 40

Proteinuria
damage/dysfunction in one of the components of the glomerular filtration barrier can result in passage of albumin/other proteins into plasma filtrate and final urine
injury to proximal tubular cells may result in the presence of low-molecular-weight proteins and/or peptides in the final urine
Peripheral edema
Due to major perturbations that favor net filtration out of the plasma into the interstitium like:
increased capillary hydrostatic pressure (from increased venous pressure) seen in expansion of plasma volume due to sodium retention (heart, liver, kidney disease), central or regional venous obstruction
decreased plasma oncotic pressure from reduced albumin
increased interstitial oncotic pressure from changes in conc of mucopolysaccharides and filtered proteins, capillary wall permeability (inflammatory response), rate of lymphatic clearance
diffusion of sodium and water out of the vasculature and into the interstitial space results in activation of the renin-angiotensin system and further renal retention of sodium and water to maintain normal blood volume
underfill hypothesis (intravascular volume depletion) vs overfill hypothesis (intravascular volume expansion; more favored)
Hyper-coagulable state
Shift in balance between antithrombotic and prothrombotic activities d/t urinary loss of proteins that prevent thrombosis as a result of altered permselectivity of gbm, incr production of factors that promote thrombosis, reduced fibrinolysis activity due to loss of plasminogen and regulator of plasmin formation, mild thrombocytosis and platelet hyperreactivity from increased ncreased levels of vWf, hyperfibrinogenemia, hypercholesterolemia, and hypoalbuminemia
risk factors: membranous nephropathy, age > 60 years, high creatinine level, and long prothrombin time

Question 41

Nephrotic Syndrome SXS

Answer 41

Typically: progressive lower extremity edema + fatigue
SOB with or without chest pain (from pleural effusion or ascites)
periorbital edema (often first sign)
genital edema
ascites
hypertension
pleural effusion
pericardial effusion
fluid overload
eruptive xanthomata
frothy urine
thromboembolic event
In secondary causes - nephrotic syndrome 1 of multiple disease manifestations

Question 42

Nephrotic Syndrome DX

Answer 42

proteinuria > 3.5 g/24-hour urine or spot urine protein to creatinine ratio > 3,000-3,500 mg/g (300-350 mg/mmol)
peripheral edema on physical exam
serum albumin < 2.5-3 g/dL (25-30 g/L)
Routine blood tests: serum albumin and total protein must be low, LFTs, coags, lipid panel, CBC, tests for bone and mineral disorders such as calcium (corrected serum calcium if albumin low), phosphorus, parathyroid hormone, and alkaline phosphatase
+- others: CRP, ESR, aPLA2R) to assess for primary membranous nephropathy, total immunoglobulins and serum protein electrophoresis with immunofixation (if amyloidosis or multiple myeloma is suspected), hepatitis B virus (HBV) and hepatitis C serology, cryoglobulins, HIV test, HbA1c, AI screen; ANA, anti-ds DNA, complement C3 and C4 levels, RPR
Urine studies: midstream urine to rule out infection - microscopy, culture/sensitivity
random urine sample (first morning void); assess spot protein to creatinine ratio or albumin to creatinine ratio - faster + just as accurate as 24 hr collection
+- imaging: CXR, abdominal or renal US, doppler US, CT/MRI if renal vein thrombosis suspected, CTPA
potentially determine the renal pathology with kidney biopsy (when cause unclear) ex uncontrolled diabetes (presence of enlarged kidneys, bland urinary sediment without cellular casts, or other evidence of microvascular disease) consult nephro!

Question 43

Nephrotic Syndrome TX

Answer 43

Treat complications, manage clinical manifestations, treat underlying cause
- reduce proteinuria by treating primary disease + decrease in glomerular htn/podocyte damage with ACE/ARB (+- spirinolactone, HCTZ); adequate protein intake + high carb diet rec
- reduce edema by limiting dietary sodium double dose every 1-3 days; if refractory > IV diuretics or add thiazide-type diuretics, potassium-sparing diuretics, or metolazone
+- albumin-enhanced diuresis in refractory edema with serum albumin < 2 g/dL in patients who fail restriction of sodium intake and diuretic therapy
high risk of clotting - prophylactic AC
full dose if with clot or serum albumin is < 2-2.5 g/dL with ≥ 1 of the following:
proteinuria > 10 g/day
body mass index (BMI) > 35 kg/m2
family history of thromboembolism with known genetic risk
New York Heart Association Class III or IV congestive heart failure
recent abdominal or orthopedic surgery
prolonged immobilization

Statins for HLD
Management of underlying kidney pathology mainly w immunosuppressive therapy

Question 44

Nephrotic syndrome complications

Answer 44

Many complications believed to result from overproduction of hepatic proteins and loss of low-molecular-weight proteins in urine
Blood clots
Infections
AKI
CKD
Dyslipidemia

Question 45

nephritic syndrome patho

Answer 45

inflammation of glomeruli due to any causes of GN (post strep GN mc)

Question 46

nephritic syndrome lab findings

Answer 46

hematuria
AKI
Non-nephrotic range proteinuria

Question 47

nephritic syndrome SXS

Answer 47

HTN
Edema