Renal Flashcards

1
Q

Dehydration in patient who is vomiting vs SIADH

What would you see for Una, Uosm, and Serum osm?

A

Hyponatremic dehydration

  • Una is low (bc reabsorbing sodium to reabsorb water)
  • Uosm is high (bc reabsorbing water)
  • Serum osm is low (bc Na is biggest contributor to osm)

Urine sodium is an indicator of intravascular volume status and low urine sodium (< 20–25 mEq/L [20–25 mmol/L]) suggesting decreased perfusion even in patients without clinical features of dehydration (such as edematous pts in nephrotic syndrome, cirrhosis, CHF)

SIADH:

  • Una is high (bc ADH causes increased water absorbtion
  • Uosm is high
  • low serum osms (bc more water circulating)
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2
Q

Some patients with chronic renal failure have a normal GFR

A

Serum creatinine and glomerular filtration rate (GFR) are not good indicators of the loss of functioning nephrons because of the compensatory increased function in the remaining nephrons and increased tubular secretion of endogenous creatinine.

The early stages of progression of chronic kidney disease (CKD) are accompanied by minimal elevation in serum creatinine, but a major decrease in GFR.

Increasing proteinuria, albuminuria, and/or new-onset or worsening hypertension is indicative of progressive CKD despite a stable GFR (especially in the early stages of CKD).

Variable urea production in patients with renal injury and tubular urea reabsorption make blood urea nitrogen a less reliable marker for GFR than creatinine.

Normal GFR > 90

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3
Q

Causes of hypochloremia

A

Hypochloremia is seen with Met Alkalosis

Urine chloride = helps assess intravascular status.

So if Urine chloride is low (<20) likely volume depletion
- vomiting, CF with loss of chloride rich sweat

If urine chloride is high (>40),

  • renal tubular disorders with salt wasting (Bartter and Gitelman) will present with that, hypochloremia, hypoK, met alkalosis
  • primary aldosteronism - HTN, hypoK, and meta alkalosis with high urinary chloride
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4
Q

Recurrent episodes of dehydration with FHX of males being affected

A

Nephrogenic DI

  • ADH-R mutation is X-linked
  • neonates with irritability, FTT< dehydration
  • Hypernatremia with low urine osmolality

Other cuases of increased free water loss: diabetes mellitus (osmotic diuresis), diabetes insipidus (DI; antidiuretic hormone disorders), and psychogenic polydipsia

Tubulointerstitial injury associated with chronic kidney disease leads to reduced urinary concentration (acquired nephrogenic DI). These patients usually present with polyuria with or without enuresis.

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5
Q

How to treat HyperK

A

Diuretics, cation exchange resins, and dialysis remove excess potassium from the body.

Intravenous calcium gluconate (10%) is indicated for patients with severe hyperkalemia (> 7.0 mEq/L), widening of the QRS complex or absent P waves, and arrhythmias assumed to be secondary to hyperkalemia.

Inhaled β-adrenergic agonists, insulin-glucose infusion, and sodium bicarbonate move serum potassium from the extracellular to the intracellular compartment.

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6
Q

Gross hematuria DDX

A

file:///Users/vicky/Downloads/C188A.pdf

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7
Q

Na and K daily requirements.

A

Energy expenditure to meet daily needs is 100 kcal/kg which is associated with 100 mL/kg of sensible and insensible fluid loss

Na = 2-3 mEq per 100mL of fluid loss
K = 1-2 mEq per 100mL of fluid loss
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8
Q

Metabolic Acidosis

A

Anion gap (NA - HCO3 - Cl)

Non-anion gap = 8-12

  • RTA - loss of HCO3 from urine
  • Diarrhea - loss of HCO3 from stool
  • Urine anion gap is NEG in diarrhea vs. RTA

Urine anion gap = Na + K - Cl

  • positive = low urinary NH4 (represented by Cl) = RTA
  • negative = high urinary NH4 and excretion of H = diarrhea

Anion gap > 12
MUDPILES

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9
Q

Metabolic Alkalosis

A

Increased HCO3 (due to loss of Cl)

  • Vomiting
  • Diuretics
  • Diarrhea
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10
Q

Hypertrophic Pyloric Stenosis

A

HypoCl HypoK Met Alkalosis

Can also have HypoNa!

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11
Q

Met Acidosis/Alkalosis Formulas

A

Metabolic acidosis
Winters:
pCO2 = 1.5 * HCO3 + 8 +/- 2

Resp:
HCO3 goes up 3.5 for every 10 mmHg in pCO2

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12
Q

Dehydration Tables

A

Mild-Mod-Severe: file:///Users/vicky/Downloads/C81A.pdf

ORS: file:///Users/vicky/Downloads/C81B.pdf

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13
Q

Respiratory Acidosis Compensation

A

In the acute phase of respiratory acidosis, serum bicarbonate rises slightly (approximately 1 mmol/L for every 10 mm Hg of increased partial pressure of carbon dioxide [Pco2]) due to buffering by intracellular proteins.
AKA carbonic anhydrase reaction
H2O + CO2 ↔ H2CO3 ↔ H+ + HCO3-

In the chronic phase of respiratory acidosis, over days or longer, serum bicarbonate rises approximately 3.5 mmol/L for every 10 mm Hg of increased Pco2, because of the increased reabsorption of bicarbonate at the renal tubular level.

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14
Q

Hypernatremic Dehydration

A

Hypernatremic dehydration

  • with gastrointestinal losses is more frequently associated with decreased water intake that occurs in patients with altered sensorium (ie, developmental delay) or infants who receive inadequate fluid intake from their caregivers
  • diabetes mellitus
  • diabetes insipidus

Sx: underestimation of the degree of dehydration.

Neurologic sequelae are frequently seen in infants with hypernatremic dehydration*

Free water deficit: 0.6 x wt x Na/140-1
Rate of lowering: 10 to 12 mEq/L/d (0.4-0.5 mEq/L/h) over 48 to 72 hours. to prevent cerebral edema

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15
Q

Hyponatremia

A

Plasma osmolality is tightly controlled between 280 and 295 mOsm/kg by osmostatic mechanisms in the posterior pituitary gland through regulation of the thirst mechanism and antidiuretic hormone (ADH).
mOSm/kg = 2NA + BUN/2.8 + Glucose/18

Increased ADH secretion:
- CHF, SIADH, neurologic conditions like TBI or surgery, pulmonary infections

Hypertonic HypoNa
- pseudohyponatremia = occurs in DKA when theres lots of glucose and it draws water out of cells

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16
Q

Alport Syndrome

A

Alport syndrome is an inherited disorder (often X-linked) of basement membrane collagen characterized by involvement of the kidneys (always), ears (often), and eyes (occasionally).

Sx: recurrent episodes of hematuria is the earliest manifestation and a universal symptom in patients with Alport syndrome.

In affected males, ESRD is common by 30 years of age. Females rarely develop end-stage renal disease but may still have intermittent microscopic hematuria.

VS: Asymptomatic isolated microscopic hematuria frequently seen in children, is usually transient and benign in etiology.

Anterior lenticonus is the conical protrusion of the lens and is pathognomonic of AS.

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17
Q

Renal stones - most common identified cause

A

Hypercalciuria
- Less commonly cystine, oxalate, and uric acid renal stones.

Urinary metabolic abnormality is the most commonly identified risk factor for renal stones. So should eval all pts with stones for this, with 24 hour urine collection.

Increased urinary excretion of citrate (most important), magnesium, and pyrophosphate is associated with decreased risk for renal stone formation, and a low level of these inhibitors is associated with an increased risk for nephrolithiasis in children and adults.

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18
Q

Prune Belly Syndrome

A

Triad of:

  • undescended testes
  • GU abnormalities/renal dysplasia
  • abnl abd wall musculature
  • > oligohydramnios -> lung hypoplasia
19
Q

Osmolar gap

A

Measured - calculated serum osm

Calculated = 2Na + BUN/2.8 + Glu/18
> 10 = high osmolar gap (exogenous acid)
< 10 = normal (endogenous acid like ketoacid)

20
Q

RTA - non anion gap met acidsois

A
Type 1: Distal 
- can't excrete H+
- pH alkalotic > 5.5
- hypoK 
=> inhalants

Type II: Prox

  • can’t reabsorb bicarc
  • pH normal bc still H in there, so < 5.5

Type IV: resistance to aldo
- HYPERK

21
Q

Poststrep glomerulonephritis - antibodies

A
Impetigo/Skin = Anti-deoxyribonuclease B (DNase B).
Pharyngeal = Anti-streptolysin (ASO)
22
Q

Pseudohyperkalemia

A

Hemolysis in the tube
Thrombocytopenia
Leukocytosis

23
Q

What electrolyte abnl in immobilizations?

A

Hyper CALCEMIA

  • Stones, Bones, ABD GROANS, PSYCHIATRIC OVERTONES
  • SHORTENED QT interval!!
24
Q

EKG changes for electrolytes:

A

HyperK - prolonged QRS, ST-T, peaked T, absence p waves
HypoK - prolonged PR, ST-T, prolonged QT

HypoCa - prolonged QT, AV block
HyperCa - shortened QT

HyperMag- prolonged QT, AV block

25
Q

Dietary management for stones

A
  • generous fluid intake
  • decreased salt intake
  • pharmacological therapy with HCTZ (hydrochlorothiazide) when hypercalciuria is significant
  • decrease vitamin C (vit C increases urine oxalate)
  • INCREASE Ca! (binds the oxalate)
  • decrease oxalate
26
Q

Nail-Patella Syndrome

A

Auto Dom

  • Absent, hypoplastic, dystrophic nails
  • Knee pain and patellar dislocation
  • RENAL disease - proteinuria with or without hematuria in up to 50% of patients. Progression to end-stage renal disease occurs in approximately 15% of affected individuals, usually in the 3rd or 4th decade of life.
27
Q

Screening for Diabetic Nephropathy

A

Urine microalbumin (UA is not sens enough)
DM Type 2 - at diagnosis
DM Type 1 - 5 years after the initial diagnosis
Then yearly

28
Q

Persistent Hematuria

A

Familial Hematuria

  • persistent hematuria without proteinuria
  • Autosomal Dom - TEST PARENTS
  • Benign if no FHX of ESRD or deafness

Hypercalciuria

  • renal stone formation
  • U Ca/Cr > 0.2
29
Q

Gross Hematuria

A

There will be a recognizable and apparent cause for gross hematuria!! Unlike with microscopic hematuria

DDX: UTI, cystitis, trauma, crystalluria, stones

If asymptomatic, then usually require workup:
- urinalysis with microscopy (to differentiate between RBC and heme pigments)
urine calcium-creatinine ratio (for hypercalciuria)
- serum creatinine and C3 levels (for nephritis)
- renal ultrasonography (for congenital anomalies or bladder mass)
- hemoglobin electrophoresis (for sickle cell disease)

30
Q

Polycystic Kidney Disease

A

AR = associated with portal fibrosis

  • detected on prenatal ultrasound.
  • can result in potter syndrome
  • assoc. with congenital hepatic fibrosis and portal HTN
  • US: large, echogenic kidneys with decreased corticomedullary differentiation

AD = associated with intracranial aneurysms

  • children are asymptomatic -> symptoms in adulthood
  • if has symptoms - persistent micro hematuria, HTN, flank pain (from cyst hemorrhage), or UTI
  • usually dx’ed incidentally OR screening with renal US for family hx
  • US: macrocysts
  • serum creatinine normal b/c renal fxn is normal until 30s
  • extrarenal manifestations: cerebral aneurysms, hepatic/pancreatic/seminal vesicle cyst, diverticula, abd wall hernia
31
Q

HTN, hypokalemia, met alkalosis = what syndrome

A

Liddle syndrome (pseudoaldosteronism)

  • AD
  • increase in Na reabsorption and K secretion in collecting tubule
32
Q

Hypokalemia and met alkalosis but NO HTN = what syndromes

A

Renal tubular disorders - Bartter and Gitelman

  • HypoK
  • Met Alkalosis
  • High urinary chloride
33
Q

PUV vs. other etiologies

A

Posterior urethral valves are identified on prenatal ultrasonography in most cases -> Potter sequence

Ultrasonographic findings of bilateral hydronephrosis, dilated bladder, thickened bladder wall, and a dilated posterior urethra in male patients are highly suggestive of underlying posterior urethral valves.

Need to be followed even after correction bc renal failure can still occur from renal dysplasia/injury

VS.
Unilateral hydronephrosis:
ureteropelvic junction
ureterovesical junction

No thickened bladder wall:
VUR, and ureteropelvic, ureterovesical junction

34
Q

Multicystic Dysplastic Kidney

A

“unilateral flank mass” with noncommunicating cysts with thin-no parenchyma and dysplasia

It is UNILATERAL and associated with urinary tract anomalies - so get a renal US and VCUG

Most have normal renal function with compensatory hypertrophy of the other kidney.

35
Q

VUR

A

Spontaneous resolution:
- low grade, unilateral I to IV, prenatal hydronephrosis, and diagnosis before age 1

Not likely to have spontan resolution:

  • ANY grade V, uni or b/l
  • Bilateral Grade III-IV

Antibiotic prophylaxis is recommended for children with high-grade reflux, recurrent urinary tract infection, bladder or bowel dysfunction, or obstructive uropathy.

36
Q

Pediatric HTN

A

Normal <120/80 or 90th %
Elevated 120-129/80-80 or btwn 90-95%
Stage I 130-139/80-89 or >/= 95%
Stage II 140/90 or >/= 95+12

LIfestyle Modifications!!

Stage I: Also Rpt in 3 months, then if high, ABPM, and then if still stage I then meds

Elevated BP: Rpt in 6 months

37
Q

CKD

A

< 60 mL/min/1.73 m2 for greater than 3 months regardless of whether other CKD markers are present

> 60 mL/min/1.73 m2 + evidence of structural damage or other markers of functional kidney abnormalities including proteinuria, albuminuria, renal tubular disorders, or pathologic abnormalities detected by histology or inferred by imaging

38
Q

Renal Transplant

A

Renal Transplant is treatment of choice for RRT

No significant advantage of hemodialysis over peritoneal dialysis.

39
Q

How to differentiate diarrhea from RTA?

A

Urinary anion gap
Na + K - Cl = surrogate marker for urinary ammonium excretion

Diarrhea:

  • Negative urinary anion gap (aka normal urinary ammonia production)
  • You reabsorb HCO3, and in the process need NH4Cl to buffer the H that you excrete.
  • This increases the Cl in urine and leads to negative urinary anion gap!
40
Q

What transplant drug causes HTN?

A

Tacrolimus - calcineurin inhibitor

Drugs that cause hypertension include corticosteroids, decongestants, nonsteroidal anti-inflammatory medications, herbal supplements, β-adrenergic agonists, erythropoietin, cyclosporine, tacrolimus, and stimulants (attention-deficit disorder medications).

41
Q

Flank mass, thrombocytopenia, hematuria

A

Renal vein thrombosis!!

42
Q

Diabetic Nephropathy HTN treatment

A

ACEi - reduces proteinuria, and enhances renal survival.

43
Q

GPA granulomatosis with polyangitis (Wegener)

A

Necrotizing granulomatous vasculitis
Sinus, Lungs, Kidneys!
- oral/nasal/mucosal ulcers and recurrent sinusitis
- cough and hemoptysis, pulm hemorrhage, cavitary lesions
- glomerulonephritis

+ ANCA **

Tx: Pred + Methotrexate or Cyclophosphamide