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Med School > AKI > Flashcards

AKI Flashcards

1
Q

Role of kidneys

A

maintain ECF, produce erythropoietin/renin, activate vitamin D

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2
Q

What are normal GFR numbers?

A
  • ## 140 in men, 126 in women
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3
Q

How to calculate urinary clearance? What is an ideal urinary clearance measure? Why is 24h CrCl not used?

A

UV/PT (urinary conc. x urine volume/ plasma conc. x time of urine collection)

  • inulin is gold standard but serum creatinine measured clinically (constant, small, freely filtered)
  • it overestimates GFR especially at low values - as kidney function decreases more creatinine is secreted by the kidney tubules
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4
Q

Failings of serum creatinine measurement?

A
  • people have different muscle mass, meat diet, etc.
    -insensitive to GFR decreases, especially in early stages as nephrons are initially hyperfiltrating
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5
Q

Which GFR equation is used? Limitations?

A
  • CKD-EPI –> more accurate for normal GFR >60
  • less accurate for extremes of age and body size, para/quadripelegia, amputation, skeletal muscle diseases, pregnancy, CANNOT USE IF AKI
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6
Q

CKD Categories (CGA)

A

Stage 1,2,3a,3b,4,5 based on GFR (1 is above 90 and 5 is below 15)

Stage A1/2/3 based on albuminuria (ACR)
- normal/ mild is under 30 (mg/g) or 3 (mg/mmol)
- moderate is 30-300, 3-30
- severe is 300+, 30+

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7
Q

What could cause a transient increase in albuminuria?

A
  • fever, inflammation, exercise, meds, hyperglycemia
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8
Q

If a man has to secrete 600mosm/day of solute, how much urine should he secrete if
- in the desert
- force fed water

A
  • 600/1200 = 0.5L (as concentrated as possible)
  • 600/50 = 12L (as dilute as possible)

*normal urine concentration is between 50-1200mosm/kg

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9
Q

Definition of AKI (Stage 1/2/3)

A

An acute (48h) rise in creatinine –> over 26umol/L increase or 1.5x baseline.

Can also include urine output, though less definitive (kidneys can produce normal amounts of urine despite dysfunction).
1 –> under 0.5ml/kg/h for 6-12 hours
2 –> under 0.5ml/kg/h for 12+ hours
3 –> under 0.3ml/kg/h for over 24 hours OR anuria for 12 hours

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10
Q

Post-Renal AKI
How do you test for it?
Treatment?

A
  • Anything that impairs urinary outflow –> back up of urine leads to hydronephrosis/ distended renal pelvises and calyces –> can lead to chronic obstructive nephropathy

Intraluminal –> stones, clots, tumors, abscesses
Extra luminal –> tumors, abscesses, fluid, LNs, vessels
- i.e. prostate hypertrophy, urethral stricture/ stenosis

  • Rule out with foley catheter (lower) or nephrostomy tube (upper) and renal U/S
  • Decompression before dialysis
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11
Q

Pre-Renal AKI
Treatment?

A
  • Anything that impairs renal perfusion
  • Absolute Decreased ECF –> diarrhea/vomiting, poor oral intake, diuretics, blood loss
  • low JVP and hypotension
  • Effective Decreased ECF –> impaired CO, shock, altered hepatorenal flow (i.e Hep C leading to vasodilation, fluid moving to interstitial space, and renal constriction) NSAIDs and ACEis that decrease intra-glomerular pressure
  • edema, high JVP, and ascites
  • solve the underlying problem (stop NSAIDs, five fluids)
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12
Q

Intrinsic AKI

A
  • An anomaly inside the kidney (vascular, glomerular, intersitital, tubes)
  • Most commonly acute tubular necrosis (ATN) –> decreased flow and O2 leads to PGs/NO/TGF/etc.

Ischemic ATN –> sepsis, shock, meds, lower BP, ischemia, up to 3 months

Toxic ATN –> contrast, antimicrobials, chemotherapeutics, myoglobin from rhabdomyolysis, uric acid
- typically non-oliguric, days

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13
Q

What can lead to oliguria?

A

decreased flow, increased intratubular pressure, increased Na distally (all decrease GFR)

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14
Q

Indications for dialysis

A
  • persistence of severe AKI consequences despite treatment, OR toxic ingestion/ decreased LOC
  • pulmonary edema (respiratory failure), acidemia (cardiac standstill), hyperkalemia (lethal arrythmias i.e. peaked T, wide QRS, Vfib), pericarditis, encephalopathy/ seizures
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15
Q

What do you give to a hyperkalemic patient experiencing arrythmias?

A

Calcium gluconate

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16
Q

Urinalysis signs of glomerulonephritis

A

red cells, red cell casts, protein

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17
Q

Indications for kidney biopsy

A
  • unexplained progressive AKI
  • evidence of glomerular or systemic disease
  • potential genetic cause (Alport’s)
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18
Q

Proper collection technique for a urine sample?

A

First thing in the morning, midstream, clean and sterile container, analyze within 1-2 hours

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19
Q

What can different colours of urine indicate? What does frothy urine indicate?

A

Black –> Hgb, Mgb, homogenistic acid
White –> pyuria, propofol
Green/ Blue –> pseudomonas, methylene blue, propofol
Purple –> bacturia w catheters
Orange/red –> phenazopyridine
Pink/red/brown –> blood, Hgb, Mgb, beets, rifampin

frothy urine indicates proteins

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20
Q

What is normal urine pH?

A
  • 4.5-8
  • can be more acidic if protein, acidosis
  • can be more basic if vegetarian, citrus, UTI, alkalosis
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21
Q

What is specific gravity? What could high or low values indicate?

A
  • ratio of urine density: equal volume of H20 (measures concentrating ability)
  • 1.003 (dilute) to 1.035 (concentrated)
    Low –> increased fluids, diuretics, DI
    High –> dehydration, SIADH
    Fixed –> severe renal disease
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22
Q

What is measured on urine macroscopy (dipstick)?

A

pH, specific gravity, blood (peroxidase activity of RBCs/Hgb/Mgb, need confirmation with microscopy), protein, glucose, ketones, nitrite, leukocyte esterase

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23
Q

Measuring protein in urine - what exactly are you measuring?

A
  • mostly sensitive to albumin, not senstitive enough to detect microalbuminuria
  • graded negative to 4+
  • dilute urine may underestimate proteinuria (and vv)
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24
Q

Why would you see glucose in urine? Ketones? Leukocyte esterase?

A

Glucose –> filtered load exceeds resorptive capacity of tubules (over 10mM) OR defect in resorption (under 10 mM)

Ketones –> diabetes, starvation, alcoholic ketoacidosis (does not detect B-hydoxybutyrate which is 80% of ketones)

Leukocyte esterase –> enzyme in neutrophils/ macrophages, see if intact/lysed WBCs (infxn, inflamm, malignancy, stones, glomerunephritis)

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25
Q

What would cause a false (+) vs false (-) nitrite?

A

False (+) –> bacteria (especially enterobacter), delayed, bad storage

False (-) –> low nitrite diet, ABX

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26
Q

RBC and WBC findings on urine microscopy
- normal values
- what can cause them to be increased

A

RBC –> normal is under 3
- can be more if exercise, trauma, stones, infxns, malignancies, glomnephritis

WBC –> normal is under 5
- can be more if infxn, inflamm

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27
Q

Renal tubular epithelial cells
Transitional epithelial cells
Squamous epithetial cells

Normal values? What can cause them to be increased?

A

Renal tubular –> normal is under 2
- can be more if ATN, nephritis, etc.

Transitional Epithelial –> a few is normal
- SUPERFICIAL (large, circular, small nucleus) common with UTI
- DEEP (small, oval, large nucleus) common with bladder cancer and stones

Squamous –> insignificant! genital contamination

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28
Q

Oval fat bodies
Bacteria
Yeast
Free lipid droplets

A

Oval fat bodies –> nephrotic syndrome
Bacteria –> infection or contamination, normally <10
Yeast –> infection or contamination
Free lipid –> nephrotic syndrome, trauma, contamination

29
Q

What are casts? What can different types of casts indicate?

Hyaline, granular, waxy, broad, RBC, WBC, RTE, fatty

A
  • Tamm-Horsfall mucoproteins and trapped elements
  • Hyaline - no cells only mucoproteins, non-specific
  • granular/ waxy - non-specific
    Broad - diluted renal tubules (advanced CKD, ESRD)
  • RBC - glomerulonephritis
  • WBC - pyelonephritis, acute interstitial nephritis, glomerulonephritis
  • RTE - ATN, nephrotoxins, transplant rejection
  • Fatty - nephrotic syndrome
30
Q

What are crystals? What are examples of pathological crystals?

A
  • formed when urine is supersaturated

Cystine - cystinuria (defect in proximal tubules)
Cholesterol - nephrotic syndrome
Bilirubin - severe liver disease
Drug - overdose, dehydration, hypoalbuminemia

31
Q

Overflow vs Post-renal vs Tubular proteinuria?

A

Overflow –> excess proteins in serum that exceeds resorptive capacities (Mgb suggests rhabdo, Hgb suggests hemolysis, Ig light chains suggests multiple myeloma)

Post-renal –> infxn/ inflammation/ stones/ tumours of the lower tract

Tubular –> interference with proximal tubule reabsorption

32
Q

ACR

A
  • urine albumin to creatinine ratio
  • useful for prognosis, Dx of diabetic nephropathy, CKD staging
33
Q

Spot vs 24h urine

A

Spot –> dipstick, ACR, PCR (protein), urine protein electrophoresis (for MM), 1ST LINE

24h –> albumin and protein excretion rate, urine protein electrophoresis

34
Q

Urine findings for:
- Glomerulonephritis
- Nephrotic syndrome
- Acute Pyelonephritis
- Lower UTI
- ATN
- DM
- Carcinoma

A

Glom - turbid, blood/protein, RBC (casts), WBC (casts), RTE casts

Nephrotic - frothy, lots of protein, fatty casts, oval bodies, cholesterol crystals

Pyelonephritis - turbid, nitrite, leukocyte esterase, WBC (casts), bacteria

Lower UTI - same as pyelonephritis + transitional epithelial cells and NO casts

ATN - isotonic urine (fixed specific gravity) in a hypotensive patient

DM - glucosuria, ketonuria, nocturia, dehydration

Carcinoma - atypical urothelial cells and RBCs

35
Q

Glomerular filtration barrier

A
  • fenestrated endothelial cells, glomerular basement membrane, podocytes (slit diaphragm)
  • prevent filtration of larger (-) proteins
36
Q

Glomerulonephritis
- cause
- dx/tx
- etiology

A
  • immune injury to glomerulus
  • dx: kidney biopsy
  • tx: immumnosuppresives
  • either NEPHROTIC (isolated barrier injury) or NEPHRITIC (diffuse inflammation)
37
Q

Nephrotic Syndrome
- signs?
- most common cause?

A
  • a lot of protein in the urine (>3.5)
  • hypoalbuminemia, hypercholesterolemia
  • peripheral edema (loss of oncotic pressure)
  • hypercoaguability (VTE), infection (loss of Ig),
  • AKI (proteinuria damage, interstitial edema)
  • Lipiduria (oval bodies, fatty casts
  • most common cause is diabetic nephropathy
  • can also be caused by membranous nephropathy (MN), FSGS, MCD, etc.
38
Q

Nephritic Syndrome
- signs?
- causes?

A
  • RBCs, RBC casts, dysmorphic RBCs
  • proteinuria and edema is less severe than in nephrotic, but GFR will decrease faster and earlier on than nephrotic

Based on direct IgG immunofluorescence staining…
Pauci-immune –> ANCA vasculitis
Linear staining –> Goodpasture’s (anti-GBM Ab)
Granular immune complex –> SLE, IgA, autoimmune

39
Q

Immune mediated glomerular injury
- 3 main mechanisms
- subendothelial vs subepithelial vs mesangial

A
  • Ag-Ab immune complexes
    1. Circulating IC (passive deposition in glomerulus)
    2. Circulating Ag (in-situ Ab binding)
    3. Ab targets self-AG in the glomerulus

Subendothelial (most inflamm) > mesangial > subepithelial (little inflamm as no access to circulation)

40
Q

Non-immune mediated glomerular injury

A
  • glomerular sclerosis and interstitial fibrosis
  • remaining healthy nephrons must increase their GFR
  • angiotensin II causes vasoconstriction of the EA>AA, this helps maintain GFR initially but long term leads to glomerular damage
41
Q

Pyelonephritis vs cystitis
Colonization vs ascension

A
  • infection of the kidney/ renal parenchyma (upper) vs infexion of the bladder (lower)
  • movement from urethra to bladder vs. movement from ureter to kidney (via fimbria attaching to uroepithelium)
42
Q

UTI Risk factors

A

indwelling catheter, ABX, spermicides, voiding disfunction, female (shorter urethra), sex, pregnancy, vesicouretal reflux (urinary retention)

43
Q

UTI Sx

A

dysuria, frequency, hematuria, suprapubic tenderness, chills/fever, flank pain and CVA tenderness

*malodorous/ cloudy urine or mental status change is NOT specific to UTI
* leukocyte esterase/nitrite also poor Sn/Sp

44
Q

Which pathogen most commonly causes UTIs?

A
  • E. coli
  • things like pseudomonas and enterobacter are more likely if hospital-acquired
45
Q

When should you order a blood culture for UTI?
When should you collect urine?

A
  • only collect blood if sepsis/ shock/ fever/ immunocompromised
  • DO NOT collect urine/culture unless symptomatic UNLESS pregnant/ instrumented (also do not give ABX in this scenario)
46
Q

Treatment for Cystitis vs pyelonephritis

A

Cystitis –> nitrofurantoin (5 days) or fosfomycin (1 dose)

Pyleonephritis –> IV ceftriaxone or gentamicin
–> oral cefixime or amox-clav or TMP-SMX
–> if ER/ septic, ceftriaxone or gentamicin

*shortest duration possible, change to oral ASAP, remove catheter ASAP, hydrate

47
Q

Role of:
Proximal tubule
Loop of Henle
Distal tubule
Collecting tubule

A

Proximal –> reabsorbs 65% NaCl/H20/K, 90% HCO3-, glucose and amino acids

LOH –> reabsorbs 35% NaCl/H20 (countercurrent multiplier), 25% K in ascending loop

Distal Tubule –> reabsorbs 5% NaCl, almost no H20

Collecting Tubule –> principal cells reabsorb Na+ and Cl- and secrete K+ via aldosterone
- intercalated cells reabsorb K+ and secrete H+
- will reabsorb more water in the presence of ADH

48
Q

What is normal serum K? Where is it located? What is it needed for? How is it excreted/ managed?

A
  • 3.5-5
  • most abundant intracellular cation, important for nerve conduction and muscle contraction
  • whatever is ingested must be excreted, mainly excreted in urine. Controlled by SECRETION, not by reabsorption.
  • kidney however cannot handle minute to minute, so Na/K ATPase on principal cells and EVERY cell in the body modulates small changes in ECF potassium
49
Q

How do insulin and B-adrenergic catecholamines affect potassium?

A
  • they stimulate the pump to drive K intracellularly
  • done after a meal to avoid hyperkalemia
50
Q

Where is the main site of K+ secretion?
What is K reabsorption dependent on?

A
  • Main site of secretion is the CCD (influenced by aldosterone/ flow/ Na/ pH)
  • reabsorption is linked to Na (i.e. water absorption driven by Na, NaK2Cl cotransporter in LOH)
51
Q

Effect of Aldosterone
- what stimulates it?

A
  • increases Na reabsorption and K secretion
  • released from adrenal gland due to hyperkalemia and hypovolemia
  • activates ENaC and new ENaC production (brings Na into cells so ATPase can work)
  • increases Na/K ATPase activity
  • more (-) lumen which increases secretion of K into the lumen
  • stimulates ROMK channels on luminal membrane (secretes K into the lumen to be excreted)
52
Q

Effect alkalosis has on potassium?

A

low H+ causes shift of H out of principal cells and K into principal cells which results in increased K secretion (hypokalemia)

53
Q

Effect a full ECV has on potassium?

A
  • increased flow rate allows for delivery of more Na distally, which increases Na reabsorption and thus K secretion
  • lower flow in the CCD would result in less K excreted
54
Q

Definition of hyperkalemia
Sx
Causes
Tx

A
  • K over 5, dangerous if over 6
  • weakness, nausea, paresthesias, peaked T waves, wide PR and QRS, Vfib, etc.
  1. Increased intake - usually not the only reason
  2. Shift/Redistribution - decreased insulin, B-blockers, metabolic acidosis, digoxin toxicity, cell breakdown (rhabdo, hemolysis, tumors)
  3. Decreased Excretion - low GFR, low ECV, hypoaldosteronism (ACEis, ARBs, heparin, spironolactone)

Tx –> calcium gluconate, calcium chloride, insulin, B-agonists, bicarbonate, Kayexalate, diuertics, dialysis

55
Q

Defintion of hypokalemia
Sx
Causes
Tx

A
  • K under 3.5, dangerous if under 2.5
  • weakness, cramping, ileus, U waves, VT/VF
  1. Decreased intake
  2. Shift - B-agonists, insulin, anabolism, metabolic alkalosis
  3. Increased loss - diarrhea, laxatives, ileostomy, hyperaldosteronism (cushings, HTN, liver failure), hypomagnesia (releases inhibition of ROMK), loop/thiazide diuretics, aminoglycosides

Tx –> replace ORALLY (IV is hard), assess Mg/PO4 and consider replacing (Mg inhibits ROMK)
*SERUM potassium is not a reliable index for deficit!

56
Q

In HYPOkalemia what would a transtubular protein gradient of over 7 vs under 3 mean?

A

over 7 –> renal loss
under 3 –> extrarenal loss (GI)

57
Q

What are complications of dialysis?

A
  • hypotension, arrythmias, thrombosis, sepsis, bleeding (especially if on heparin)
  • more and earlier is not necessarily better
58
Q

What are biomarkers of AKI? How can you differentiate between AKI and CKD?

A
  • NGA1, KIM-1, Il-18, Cystatin C
  • only a kidney biopsy can differentiate
59
Q

What is the most common cause of AKI in hospital? Outpatient?

A

Hospital –> ATN
Outpatient –> pre-renal

60
Q

What urinalysis finding should always be seen by urology?

A

Gross hematuria (visibly red urine)

*gross PAINLESS hematuria is malignancy until proven otherwise

61
Q

Most common cause of AKI by age
0-20
20-40
40-60
60+

A

0-20: glomerulonephritis
20-40: UTI
40-60: bladder tumor (or UTI if female)
60+: prostate hyperplasia

62
Q

Risks for urothelial tumors?
Dx
Most common bladder cancer?
Tx

A
  • SMOKING #1, aniline dyes (painter, hairdresser), radiation, chronic cystitis (catheters, infxns)
  • Dx –> cystoscopy and biopsy (lesion and detrusor muscle for staging –> TIS, TA, T1 non-invasive, T2-T4 if invasive, T4 has spread to other organs)
  • most common is urothelial (transitional cell)
  • if non-muscle invasive –> transurethral resection, mitomycin C, chemo if high grade/ in-situ/ many lesions/ rapid recurrence
  • if muscle invasive –> radical cystectomy, chemo
63
Q

U/S
CT IVP
Cystoscopy

pros and cons

A

U/S - good for renal tumors/stones and hydronephrosis
- may miss ureter stones, smaller tumors, may just be a blood clot, no function

CT IVP - most sensitive for GU pathology, can see fluid and filling defects
- expensive, contrast, radiation (cannot give if pregnant, MM, renal dysfxn)

Cystoscopy - lower tract imaging, telescope, good for urothelial carcinomas

64
Q

Renal Mass
- signs
- labs to order
- most common malignant finding and its treatment

A
  • triad of flank pain, hematuria, and palpable mass (rare)
  • alkaline phosphatase (bone metastases), liver function, calcium (bone metastases or parneoplastic syndrome if also weight loss/fever/anemia/HTN)
  • most common malignant finding is renal cell carcinoma (clear cell)
  • Tx –> nephrectomy, chemo, targeted therapy with TK inhibitors
65
Q

Difference between pseudo-tumours and tumours on DMSA scan?

A

Tumors will have decreased uptake

66
Q

Renal Colic
- what are potential life threatening causes?
- imaging?
- when to refer?

A
  • abdominal aortic dissection/ aneurysm, appendicitis, ectopic pregnancy, septic stone
  • plain film KUB/ CT-KUB –> stones will be radiopaque
  • refer if fever, WBC, bacturia, only onekidney, CHF, pregnancy, etc.
67
Q

Stones
- what can you give to help pass
- different kinds?

A
  • will likely pass spontaneously if small, non-obstructive stones should not cause pain
  • can give tamsulosin (flomax)

Ca Oxalate –> most common, chocolate/ nuts/ tea/ hypercalciuria
Ca phosphate –> primary hyperparathyroidism, tubular acidosis, malignancy, sarcoidosis
Uric acid –> acidic urine, gout, meat, chemo
Struvite (staghorn) –> pH > 8, infection, Mg/ammonium/ PO4/ Ca

68
Q

Treatment options for stones

A
  • hydration, NSAIDs, and Flomax (tamsulosin) IF no renal impairment, vomiting, infection

Ureter stent (double J stents)
Shockwave lithotripsy if under 2cm
Ureteroscopy and laser if bigger
Percutaneous nephrolithotomy if large and risk of bleed

69
Q

Common sites for stone formation?

A
  • ureto-pelvic junction
  • ureto-vesical junction
  • crossing of iliac artery

Med School (21 decks)

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