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LMCC (anglais) > Nephrology > Flashcards

Nephrology Flashcards

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1
Q

What is defined as microscopic hematuria?

A

Microscopic hematuria is >3RBC/rpf

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2
Q

Gross, painless hematuria is ____ until r/o

A

Bladder cancer

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3
Q

A urine that is +ve by dipstick but neg on microscopy should be suspicious for?

A

Free Hb or myoglobin

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4
Q

What is a very common cause of transient hematuria in <35yo?

A

Vigorous exercise

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5
Q

The most common causes of hematuria?

A
  • Urinary tract infections (UTIs)
  • Prostatitis
  • Urinary calculi (in adults)
  • Congenital or acquired anatomic abnormalities
  • Cancers
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6
Q

Etiology of hematuria?

A
  • Glomerular: glomeruloneophritis, IgA nephropathy, HUS, lupus
  • Infectious/Inflammatory: Pyelonephritis, Cystitis, Urethritis, Glomerulonephritis Interstitial nephritis, Tuberculosis
  • Malignancy: RCC (mainly adults), Urothelial cancer, Wilms’ tumour (mainly pediatric) Prostate cancer
  • Benign: BPH, Polyps, Exercise- induced
  • Structural: Stones, Trauma, Foreign body, Urethral stricture, Polycystic kidneys, Arteriovenous malformation, Infarct, Hydronephrosis, Fistula
  • Hematologic: Anticoagulants, Coagulation defects, Sickle cell disease, Thromboembolism
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7
Q

What are some causes of pseudohematuria?

A
  • Vaginal bleeding
  • Dyes (beets, rhodamine B in candy and juices)
  • Hemoglobin (hemolytic anemia)
  • Myoglobin (rhabdomyolysis)
  • Drugs (rifampin, phenazopyridine, phenytoin)
  • Porphyria
  • Laxatives (phenolphthalein)
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8
Q

Important aspects to gather on history for hematuria?

A
  • Timing of hematuria in urinary stream
  • Urinary obstructive symptoms and irritative symptoms
  • Last menstrual period, history of kidney stones, UTI, or previous urologic surgery
  • Hearing loss (Alport syndrome), rashes (connective tissue disorder)
  • Recent URTI, post-infectious glomerulonephritis, IgA nephropathy
  • Medications (anticoagulants, rifampin, phenazopyridine, phenytoin)
  • Risk factors for malignancy (smoking, chemical exposures, Hx of cyclophosphamide therapy, pelvic radiation)
  • FHx: Stone disease
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9
Q

Physical exam for hematuria?

A
  • Vitals (fever + HTN)
  • Abdomen (masses; flanks should be percussed for tenderness over the kidneys)
  • DRE
  • Face and extremities should be inspected for edema (suggesting a glomerular disorder)
  • Skin should be inspected for rashes (suggesting vasculitis , SLE , or immunoglobulin A–associated vasculitis).
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10
Q

Cystitis predominantly shows what on UA?

A

RBCs

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11
Q

What are the 4 Cs you test for with microscopic hematuria

A
  • 4 Cs after microscopic hematuria: culture (UTI), cytology (malignancy), CT urogram (nephrolithiasis, renal massues, filling defects), cystoscopy
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12
Q

Besides the 4Cs and microscopic UA what else should be ordered?

A
  • CBC (rule out anemia, leukocytosis), electrolytes, Cr, BUN, INR, PTT, PSA (in men >50)
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13
Q

Patients < 50 with gross hematuria or unexplained systemic symptoms require?

A

Cystoscopy +/- CT of the abdomen and pelvis.

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14
Q

If microscopic UA shows: proteinuria, dysmorphic RBC, tea/coke colour, RBC casts

A

Send to nephrology

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15
Q

If microscopic UA shows: red urine, monomorphic RBCs, no proteinuria + lower urinary tract Sx

A

Send to urology

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16
Q

Hematuria: Glomerular disorders are often accompanied by?

A

Edema, hypertension, or both; symptoms may be preceded by an infection (particularly a group A beta-hemolytic streptococcal infection in children).

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17
Q

Hematuria: Calculi usually manifest with

A

Excruciating, colicky pain

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18
Q

Hematuria: Urinary obstructive symptoms in man usually suggest

A

Prostate disease.

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19
Q

Hematuria: Urinary irritative symptoms suggest

A

Bladder or prostate infection

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20
Q

Hematuria: An abdominal mass suggests

A

Polycystic kidney disease or renal cell carcinoma .

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21
Q

Acute management of severe bladder hemorrhage

A
  • Manual irrigation via catheter with normal saline to remove clots
  • Continuous Bladder Irrigation (CBI) using large (22-26Fr) 3-way Foley to help prevent clot formation (after manual irrigation of clots)
  • Cystoscopy
  • Identify tumours or other source(s)
  • Coagulate obvious sites of bleeding or transurethral resection of tumours (under general or regional anesthesia)
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22
Q

Patients with unexplained microscopic hematuria require?

A

US

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23
Q

Definition of hyperkalemia?

A

Definition: K+ >5mmol/L

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24
Q

How to potassium excreted?

A

Urine excretion of K+ is regulated (in the CCD) and does 90% of the work, 10% is lost in poop/gut (but this can increase in CKD/diarrhea).

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25
Q

What are the symptoms + cardiac features of hyperkalemia?

A

MURDER With Tall Peak T wave

  • Muscle weakness
  • Urine, oliguria, anuria
  • Respiratory distress (hypoventilation)
  • Decreased cardiac contractility
  • EKG changes
  • Reflex (hyperreflexia)
  • Cardiac/ECG: narrow, peaked T wave (especially precordial leads) + widened QRS + wide/flat P wave + V-fib
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26
Q

Ddx of hyperkalemia?

A
  • Increased intake: Diet, KCl tabs, IV KCl, Salt substitute
  • Shift out of the cell (metabolic acidosis + diabetes/insulin deficient + beta-blockade + cellular necrosis)
  • ^release (rhabdomyolysis (breakdown of damaged skeletal muscle) + burns + tumor lysis + strenuous exercise + intravascular hemolysis)
  • Decreased output (decreased tubular flow due to renal failure or effective circulating fluid volume, OR hypoaldosteronism due to decreased renin, adrenal insufficiency, type IV RTA, ACE inhibitors, ARBs, spironolactone, NSAIDs).
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27
Q

Most common causes of high [K+] are

A
  • Reduced GFR (low flow or renal failure)
  • Medications that interfere with aldosterone
  • Hyporenin-hypoaldosteronism due to DM or CKD
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28
Q

2 major pathways leading to aldosterone secretion

A
  • Renin-angiotensin pathway arising from volume signals

- Direct stimulation via sensing of plasma potassium concentration

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29
Q

Investigations for hyperkalemia?

A
  • Basic Labs: CBCd (K and CO2) + lytes + Urea/Cr + urinalysis + urine lytes + urine osmolarity + serum osmolarity + CK
  • Special Investigations: ECG (consider if K > 6.0) + ABG/VBG (quick way to get K level)

Hypoaldosteronism Workup: serum aldosterone + plasma renin activity

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30
Q

How to stabilize the myocardium for hyperkalemia?

A

Calcium chloride 10% 10ml IV push OR calcium gluconate 10% 10ml IV push; use CaCl if hemodynamically unstable, given that gluconate must be hepatically metabolized before calcium becomes bioavailable – don’t give if K>6 due to digoxin (causes V-fib!)

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31
Q

Treatment of hyperkalemia if [K+] <6.5 and normal ECG?

A

Treat underlying cause, stop K+ intake, increase the loss of K+ via urine and/or GI tract

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32
Q

Treatment of hyperkalemia if [K+] between 6.5 and 7.0, no ECG changes?

A

Treat underlying cause, stop K+ intake, increase the loss of K+ via urine and/or GI tract + insulin

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33
Q

Treatment of hyperkalemia if [K+] >7.0 and/or ECG changes?

A

Treat underlying cause, stop K+ intake, increase the loss of K+ via urine and/or GI tract + insulin + calcium gluconate

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34
Q

Besides D50W (dextrose) 50ml IV push followed by Humulin R (insulin) what else could you do to shift K into the cells for hyperkalemia?

A
  • Consider high dose beta agonist (Ventolin) - onset of action 30-90 min, stimulates Na+/K+ ATPase
  • Consider bicarbonate if severe metabolic acidosis, drives K+ into cells in exchange for H+
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35
Q

How to shift K into the cells for hyperkalemia?

A

D50W (dextrose) 50ml IV push followed by Humulin R (insulin) 10U in 50ml of D50% IV bolus; consider dextrose drip or second amp of D50W as hypoglycemia occurs in up to 70% of cases w/ 1 amp

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36
Q

How to enhance K+ removal for hyperkalemia?

A
  • Via urine (preferred) - furosemide diuretic 40mg IV, doses up to 200mg may be needed in acute renal failure
  • Via GI (if renal function is severely impaired): Cation-exchange resins: calcium resonium or sodium polystyrene sulfonate (Kayexalate®) (which is prescribed in conjunction with sorbitol)
  • Lactulose or sorbitol PO to avoid constipation (must ensure that patient has a bowel movemen tafter resin is administered - main benefit may be the diarrhea caused by lactulose)
  • Dialysis (renal failure, life threatening hyperkalemia unresponsive to therapy)
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37
Q

Which medications/drugs should be stopped with hyperkalemia?

A

Discontinue drugs like K supplements + ACEi + ARBs + spironolactone + NSAIDs + trimethoprim

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38
Q

What is the definition of hypokalemia?

A

K+ <3.5mmol/L

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39
Q

Symptoms and signs of hypokalemia?

A
  • Muscular: weakness/paralysis (periodic); may include extremities, resp/GI muscles = cramps, paresthesia, tetany, muscle tenderness, atrophy, and rhabdomyolysis may develop
  • Cardiac arrythmias
  • GI: N/V, constipation or ileus, fatigue
  • Hyperglycemia (decreased peripheral glucose uptake and impaired insulin release) + polyuria (impaired ADH)
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40
Q

Most common causes of low [K+] are

A
  • Loop or Thiazide Diuretics (increase Na+ delivery distally and induce low ECFV → high aldosterone)
  • GI fluid losses (lose K+ from the gut and induce low ECFV → high aldosterone)
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41
Q

Ddx of hypokalemia?

A
  • Decreased intake
  • Shift into the cell (metabolic alkalosis (Response: exchange of hydrogen ions for potassium from cells) + hyperinsulin states (shifts potassium into cells by stimulating the activity of Na+-H+ antiporter on cell membrane) + increased beta-adrenergic states + hypothermia)
  • Increased output
  • GI loss due to diarrhea/vomiting/tube draining/laxatives
  • Renal loss – hyperaldosteronism (Conn’s/renal artery stenosis), Non-aldosterone mineralocorticoid (Cushing’s, exogenous), Diuretics (furosemide, HCTZ) manifest as renal losses due to hyperaldosteronism, metabolic alkalosis, and increased flow to collecting duct
  • Can be drug induced (K+ supplements, ACE-i, ARB, NSAIDs) esp. with renal impairment
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42
Q

Investigations for hypokalemia?

A
  • Lytes + extended lytes (Ca/Mg/Phosphate) + Urea/Cr + urinalysis + urine lytes + urine osmolality + serum osmolarity + glucose + troponin/CK,
  • Check BP
  • Spot urine K:Cr
  • Special Investigations: ECG
  • Hyperaldosteronism Workup: serum aldosterone + plasma renin activity)
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43
Q

If spot urine K:Cr <1.5 mEq/mmol consider

A

GI loss

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44
Q

If spot urine K:Cr >1.5 mEq/mmol consider

A

Renal loss

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45
Q

Treatment for hypokalemia?

A
  • Treat underlying cause
  • If true K+ deficit, potassium repletion
  • Oral sources - food, tablets (K-DurTM), KCl liquid solutions (preferable route if the patient tolerates PO medications)
  • IV - usually KCl in saline solutions, avoid dextrose solutions (may exacerbate hypokalemia via insulin release)
  • Max 40 mmol/L via peripheral vein,60 mmol/L via central vein, max infusion 20 mmol/h
  • K+-sparing diuretics (triamterene, amiloride, spironolactone) can prevent renal K+ loss
  • Restore Mg2+ before correcting K+ - MgSO4 5g IV over 4 hours
  • Use ACE inhibitor or ARB for CHF (reduces angiotensin II action and therefore reduces aldosterone production)
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46
Q

What is the definition of proteinuria?

A

> 150mg/d of protein (usually <30mg of albumin per day, primarily Tamm Horsfall mucoprotein)

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47
Q

What is the gold standard to quantify proteinuria?

A

24 Hour Urinary Protein

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48
Q

In general, greater than 2.0g/24hr is diagnostic of ____ on dipstick (+) urine. Less than 1.0g however is unhelpful as it could be tubular or glomerular in origin.

A

Glomerular disease

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49
Q

What is commonly used to calculate how much proteinuria is present?

A

Spot Protein:Creatinine Ratio (PCR or ACR): to estimate daily protein excretion in mg

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50
Q

Normal PCR and ACR amounts?

A
  • PCR: normal is <13mg/mmol
  • ACR: normal is <2mg/mmol for men but <2.8mg/mmol for women
  • To get that 24hr amount, simply multiply the ratio by the mmols of creatinine excreted per day in the urine: for men it is 15-20, for women it is 10-15 (e.g. ACR 24 hr is 2 x 15 for man = 30). Should always be measured at the SAME TIME OF DAY (first morning void).
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51
Q

What test can you do to determine the type of proteinuria present?

A
  • UPEP (Urine protein electrophoresis helps you determine the type of protein (albumin, IgG, Tamm-Horsfaall).
  • Protein gap. If you do not have UPEP, you can compare PCR to ACR (i.e. the protein gap). E.g. if ACR low, then think about non-albumin proteinuria. If ACR is <40% of PCR – may indicate unmeasured proteins
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52
Q

Pathophysiology of proteinuria?

A
  • Glomerular Proteinuria
  • Functional proteinuria
  • Orthostatic/Postural
  • Tubular Proteinuria
  • Overflow Proteinuria
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53
Q

Causes of glomerular proteinuria?

A
  • Primary glomerular disorders (membranous nephropathy, minimal change disease, focal segmental glomerulosclerosis)
  • Secondary glomerular disorders (diabetic nephropathy, preeclampsia, postinfectious glomerulonephritis, lupus nephritis, amyloidosis)
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54
Q

The most common causes of proteinuria (and nephrotic syndrome) in adults are

A

Focal segmental glomerulosclerosis, Membranous nephropathy, Diabetic nephropathy

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55
Q

What should be asked on history for proteinuria?

A
  • Ankle swelling + fever + strenuous exercise + UTIs (FUND – frequency, urgency, nocturia, dysuria)
  • Vasculitis (rash, joint pain)
  • New diagnosis of DM
  • Connective tissue disease (Raynaud’s, photosensitivity, oral ulcers)
  • PMHx - myeloma, DM, glomerulonephropathies, SLE
  • Meds - NSAIDs/Antibiotics
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56
Q

What should be done on physical exam for proteinuria?

A
  • HEENT – periorbital edema, JVP (low in nephrotic, high in nephritic)
  • CV – pericardial rub (uremic pericarditis)
  • RESP – PE and crackles with volume overload
  • ABDO – ascites, kidney palpation
  • DERM – rash, pallor if anemic
57
Q

Causes of functional proteinuria?

A

Exercise, fever, high-output heart failure

58
Q

Causes of tubular proteinuria?

A

Fanconi syndrome, Acute tubular necrosis, Tubulointerstitial nephritis, Polycystic kidney disease

59
Q

What is glomerular proteinuria and how much proteinuria is typically present?

A

Due to increased glomerular permeability.

1-3g/d, usually >3g/d

60
Q

What is functional proteinuria and how much proteinuria is typically present?

A

Functional proteinuria occurs when increased renal blood flow delivers increased amounts of protein to the nephron, resulting in increased protein in the urine (usually < 1 g/day). Reverses when renal blood flow returns to normal.

61
Q

What is tubular proteinuria and how much proteinuria is typically present?

A

Results from renal tubulointerstitial disorders that impair reabsorption of protein by the proximal tubule, causing proteinuria (mostly from smaller proteins such as immunoglobulin light chains rather than albumin). Generally between 0.5-1.0g/24hrs.

62
Q

What is orthostatic/postural proteinuria and how much proteinuria is typically present?

A

A benign condition (most common among children and adolescents) in which proteinuria occurs mainly when the patient is upright. Thus, urine typically contains more protein during waking hours (when people are more often upright) than during sleep. Typically < 1.0g/24hr with no other abnormalities.

63
Q

What is overflow proteinuria and how much proteinuria is typically present?

A

Due to abnormal, excessive amounts of normally filtered plasma proteins.
Usually >1g/d, any amount. Glomerular barrier and tubular function intact, but amount of protein which is filtered overwhelms the normal resorptive capacity of the proximal tubular cells and the excess protein appears in the urine.

64
Q

Causes of overflow proteinuria?

A

Monoclonal gammopathy, Multiple myeloma, Myelodysplastic syndromes

65
Q

Algorithm for proteinuria?

A

Confirm presence with dipstick x2-3 → quantify with either 24hour urine OR spot (+ PCR and ACR) → identify type with UPEP or protein gap → if albumin = glomerular issue, if other = multiple myeloma (IgG) or tubular damage (Tamm-Horsfall)

66
Q

Typical presentation of minimal change disease?

A

Happens mostly in kids (classic 3-5). Present with edema but otherwise well (no hypertension or hematuria)  worry when you get pulmonary edema = respiratory distress, ascites/scrotum/peri-orbital that it impairs function

67
Q

Complications of minimal change disease?

A
  • Spontaneous peritonitis is one of the most frequent complications, with an insidious presentation of fever and minimal other findings
  • Infections – loss of IG – risk of bacterial infections from encapsulated bacteria, SBP
  • Thrombosis – intravascularly deplete, urinary loss of coagulation cascade factors, increased hepatic production of procoagulant factors
  • Renal dysfunction - AKI
  • Dyslipidemia
68
Q

Treatment of minimal change disease?

A

Fluid + salt restriction + corticosteroids (60 mg/m2 once daily x6 weeks then 40 mg/m2 once daily on alternate days x6 weeks and taper dose over 6 months). Daily urine dipsticks – in AM because of orthostatic proteinuria

69
Q

Most common pathogen for spontaneous peritonitis?

A

Streptococcus pneumoniae is the most common pathogen causing peritonitis

70
Q

Most common cause renal failure

A

Diabetic nephropathy

71
Q

Hallmarks of diabetic nephropathy?

A

Hallmarks are: mesangial expansion, GBM thickening, nodular glomerular sclerosis.

72
Q

Pathophysiology of diabetic nephropathy?

A

Hyperglycemia and hemodynamic hyperfiltration lead to IG HTN and accumulation of cytokines/end products in kidney.

73
Q

Risk factors of diabetic nephropathy?

A

Hyperglycemia, HTN, genetics! ↑GFR is worse!.

74
Q

Diagnosis of diabetic nephropathy?

A

Clinically, MICROALBUMINURIA >30mg/d. Biopsy is rarely needed.

75
Q

Screening for diabetic nephropathy?

A
  • T1DM – screen after 5 yrs with ACR + Serum Crea then ANNUALLY
  • T2DM – screen @ Dx and annually with ACR + Serum Crea + Urinalysis
76
Q

Treatment for diabetic nephropathy?

A

Glycemic control, BP control, yearly screening for microalbuminuria, smoking cessation, ACEi or ARB.

77
Q

What is membranous glomerulonephropathy?

A

Mainly adults (more common in white males >40), GBM thickened + pedicle flattening due to immune complex deposition in subepithelial space

78
Q

Disease stages for diabetic nephropathy?

A
  • Normal (<30mg/d of albumin): all good, lasts 8-10yrs.
  • Microalbuminuria (30-300mg/d or <20-28mg/mmol): marker for generalized endothelial dysfunction, increased risk or nephropathy, CV mortality, lasts 5-10 yrs.
  • Macroalbuminuria (>300mg/d or >20-28mg/mmol): relentless decline in renal function from 2-20ml/min/yr. All T1 have retinopathy and neuropathy at this stage but 50% of T2DM.
79
Q

Most common cause of nephrotic syndrome in the elderly.

A

Membranous glomerulonephropathy

80
Q

Secondary causes of membranous glomerulonephropathy?

A
  • Drugs-gold, penicillamine, captopril, NSAIDs (rarely)
  • Malignancies-esp solid tumors (lung, GI, breast)
  • Infections-hepB, syphilis, schistosomiasis
  • Collagen-vascular-lupus
81
Q

Treatment of membranous glomerulonephropathy?

A

Ponticelli protocol - IV methylprednisolone 1 g daily x 3 then prednisone 0.5 mg/kd daily x 1 month, followed by cyclophosphamide 2 mg/kg daily x 1 month, then repeat cycle for total 6 months of treatment (3 cycles each of pred and cyclophosphamide. ACEi or ARB

82
Q

What is FSGS (Focal Segmental Glomerulosclerosis)?

A

Focal (<50% glomerular involvement) segments of kidney showing scarring, all ages.

83
Q

Treatment of FSGS (Focal Segmental Glomerulosclerosis)?

A

ACEi/ARBs to reduce proteinuria because steroids take a long time to work + corticosteroids 2mg/kg alternate days or 1mg/kg daily + taper over 6 months  switch to Ci or MMF if no response/relapse

84
Q

Definition of chronic kidney disease?

A

CKD is defined as kidney disease >3mnths demonstrated by structural or functional abnormalities

  • GFR <60 mL/min/1.73 m2; or
  • Markers of kidney damage, including:
  • Hematuria, proteinuria, or anatomic abnormalities
85
Q

Causes of chronic kidney disease?

A
  • Pre-renal causes (HTN)
  • Renal causes:
  • Glomerular (IgA nephropathy, diabetic nephropathy)
  • Tubulo-interstitial (drug toxicity)
  • Ischemic
  • Congenital ( dysplasia, polycystic kidney disease)
  • Post-renal (e.g., obstructive uropathy)
86
Q

Clinical features of chronic kidney disease?

A
  • Volume overload and HTN
  • Electrolyte and acid-base balance disorders (e.g. metabolic acidosis)
  • Uremia (nausea/vomiting, pruritus, encephalopathy)
  • Anemia
  • Bone mineral disorders
  • Sleep disorders common in CKD: insomnia, sleep apnea, restless legs syndrome
87
Q

Pathophysiology of HTN causing chronic kidney disease?

A

HTN (>130/80 in these cases) – systemic HTN → vascular intimal damage → hypertrophy, narrowing of arterial lumen → chronic ischemia. Systemic hypertension leads to intraglomerular (IG) HTN, endothelial damage, podocyte detachment, and mesangial sclerosis. Other nephrons will hyper filter – more intraglomerular hypertension

88
Q

Drugs to avoid in CKD?

A
  • Metformin
  • Fibrates
  • Bisphosphonates
89
Q

Dose adjustment drugs for CKD?

A
  • Antibiotics
  • HMG CoA reductase inhibitors (statins)
  • Sulfonylureas
90
Q

Diet considerations for CKD?

A
  • Na+ restriction target of <2 g/d (5 g/d of salt), K+ restriction (40-60 mmol/d) , PO43- restriction (1 g/d), avoid extra-dietary Mg2+ (e.g. antacids)
  • Proteinuria target: <1g/day – as low as possible (low protein diet)
91
Q

HTN treatment for CKD?

A

ACEI (target 140/90 mmHg without DM and 130/80 mmHg with DM), loop diuretics when GFR <25 mL/min

92
Q

Anemia treatment for CKD?

A

Erythropoietin injections for Hb <90g/L (9g/dL) and target Hb between 90-115g/L (9-10.5g/dL). IV iron administration often required for iron deficiency

93
Q

Dyslipidemia treatment for CKD?

A

Statins (target LDL <2 mmol/L)

94
Q

Lab abnormalities for renal osteodystrophy?

A

Kidneys cannot excrete PO4 and cannot make D3 needed for Ca2+ → Leads to high PO4, low plasma Ca, and high PTH.

95
Q

Treatment for renal osteodystrophy?

A
  • Give calcium between meals (to increase Ca2+) and calcium with meals (to bind and decrease PO43-)
  • Vitamin D and calcitriol (1,25-dihydroxy-vitaminD) if hypocalcemic, but hold if hyperphosphatemic (reduces PTH)
  • Sevelamer (phosphate binder) if both hypercalcemic and hyperphosphatemic
  • PO4 restriction
96
Q

When to refer to nephrologist for CKD?

A

Prefer to have 12 months of contact with nephrologist before need for RRT due to ESRF. GFR < 30 (stage 4) → educate/risk reduction; GFR <15-20 (stage 4-5) → dialysis + transplant workup, GFR <10 (stage 5) → RRT.

97
Q

Who should be screened for CKD?

A

HTN, CAD, Diabetes, age >70, or unexplained anemia! Screen YEARLY with GFR → urinalysis/protein quant (dipstick/microscopy → PCR/ACR → UPEP + protein gap) → imaging. Biopsy if needed.

98
Q

Early manifestations of uremia?

A

Early Manifestations: nausea, anorexia, altered state, fatigue, lethargy, malaise

99
Q

When does uremia typically present?

A

Usually doesn’t appear until late. GFR < 10 ml/min

100
Q

Late manifestations of uremia?

A

Late Manifestations: nausea, vomiting daily, weight loss, peripheral neuropathy, pruritis, uremic frost

101
Q

Decision to start dialysis in ESRD should be decided based on?

A

Decision to start dialysis in ESRD should be symptom driven (uremic sx) or when GFR reaches approximately 10 mL/min or lower

102
Q

For hemodialysis or peritoneal dialysis which does success depend on residual kidney function?

A

Peritoneal dialysis

103
Q

AKIN criteria for AKI?

A

<48 hours increase in Cr of 27 U/L above baseline OR increase in Cr of 50+%, or decrease urine output of <0.5cc/kg/hr for 6 hours

104
Q

Physical exam for AKI?

A

ASSESS VOLUME STATUS

  • JVP – RA is 5cm below sternal knotch, can add to JVP height to know true height
  • Postural/orthostatic BP – change in systolic BP (drop of 20 mmHg)
  • Rash, arthritis
  • Signs of cardiac disease (HF)
  • Rectal exam as BPH is very common in post-renal
105
Q

3 main category of causes for AKI?

A
  • Pre-renal (decreased perfusion) – most common cause of AKI
  • Renal (decreased permeability or SA)
  • Post-renal (decreased outflow)
106
Q

Causes of pre-renal AKI?

A
  • Disordered Autoregulation – NSAIDs, ACEI/ARBs, Calcineurin inhibitors (cyclosporine, tacrolimus), Hypercalcemia
  • Hypovolemia
    • Absolute: Hemorrhage, GI loss, Skin loss, Renal loss
    • Effective: Low cardiac output, Cirrhosis, Sepsis, 3rd spacing
107
Q

Causes of renal AKI?

A
  • Glomerular – glomerulonephritis (nephrotic or nephritic), RPGN
  • Tubulo-interstitial – ATN, AIN
  • Vascular: Vasculitis, Malignant HTN, Thrombotic microangiopathy, Cholesterol emboli, Large vessel disease
108
Q

Causes of post-renal AKI?

A
  • Intra-tubular – multiple myeloma, uric acid crystals
  • Ureteral – bilateral stones, tumours, structures, fibrosis, malignancy
  • Bladder neck – prostate enlargement (COMMON), spasm (drugs)
  • Urethral – strictures, valves
109
Q

Investigations for AKI?

A
  • Blood work: CBC – Hgb may help with chronicity, electrolytes, Cr, urea, Ca2+, PO43-
  • Urine dipstick: albumin, hemoglobin, WBC’s, others: glucose, pH, urobilinogen, specific gravity
  • Urine volume, C&S, R&M: sediment, casts, crystals
  • Urinary indices: electrolytes, osmolality
  • Foley catheterization (rule out bladder outlet obstruction)
  • Imaging: abdomen U/S (assess kidney size, hydronephrosis, post renal obstruction)
110
Q

Indications for renal biopsy?

A
  • Diagnosis is not certain
  • Prerenal azotemia or ATN is unlikely
  • Oliguria persists >2-4 d
  • RPGN, signs of significant glomerular disease (proteinuria, RBC casts) despite normal kidney size/ echogenicity
111
Q

Clues to prerenal etiology for AKI?

A
  • Clinical: Decreased BP, increased HR, and orthostatic HR and BP changes
  • Increased [urea]&raquo_space; Increased [Cr]
  • Urine [Na+] <10-20 mmol/L
  • Urine osmolality >500 mOsm/kg – concentrating urine
  • Fractional excretion of Na+ <1% (conserving Na to get water)
112
Q

Think ____ if increase in urea is relatively greater than increase in Cr for AKI

A

Prerenal

113
Q

Clues to renal etiology for AKI?

A
  • Urinalysis positive for casts:
    Pigmented granular - ATN
    WBC - AIN
    RBC - GN
  • FENa will be >2% (urine [Na] > 40 mmol/L), plasma Cr:urea ratio 12-20:1. In pre-renal, you want to conserve salt since you have a perfusion issue so your fraction will be LOW but the opposite in a renal cause.
  • Systemic features, anemia, thrombocytopenia, HTN, mild-moderate ECF volume overload
114
Q

Clues to post-renal etiology for AKI?

A
  • Known solitary kidney
  • Older man
  • Recent retroperitoneal surgery
  • Anuria
  • Palpable bladder
  • Ultrasound shows hydronephrosis
115
Q

Management of pre-renal AKI?

A
  • IV isotonic crystalloids are preferred  RL, NS, D5NS
  • Bolus therapy more effective than maintenance therapy (risk for volume overload)
    • Low risk = 250-1000cc/hr bolus
    • Intermediate risk = 100-500 ml/hr
    • High risk = 50-250 ml/hr bolus
  • Hold ACEI/ARB (gently rehydrate when needed, e.g. CHF) and NSAIDs
116
Q

What is ATN?

A

Prolonged ischemia causing denuding of epithelium and occlusion of tubular lumen by casts and cell debris

117
Q

Causes of ATN?

A
  • Ischemia – hypotension, post-surgical, sepsis, cardiac insufficiency, drugs (NSAIDs)
  • Nephrotoxins – contrast dyes, heme pigments, Ig light chains, antibiotics (aminoglycosides), tumor lysis syndrome
118
Q

What would the urinalysis show for ATN?

A
  • <1g/d protein
  • Muddy-brown (hemegranular) casts, epithelial casts
  • Fe Na > 2% as tubules ability to conserve Na is gone
119
Q

Management of ATN?

A
  • Stop nephrotoxins, maintain renal perfusion D5-1/2-NS - Loses ability to concentrate urine for 24-48 hours
  • Manage volume, lytes, acid-base status – low potassium, fluid restricted diet
  • Remember to dose adjust meds – antibiotics, oral hypoglycemic
  • Supportive dialysis if necessary
120
Q

Renal biopsy for ATN?

A

Dilatation of PCT +/- DCT, loss of PCT brush border, normal glomeruli

121
Q

Acute dialysis indications

A

AEIOU*

  • Acidemia – uncorrectable acidosis
  • Electrolytes - Dangerous hyperkalemia (usually > 7 with ECG changes),
  • Ingestion - drugs
  • Overload - pulmonary edema unresponsive to diuretics
  • Uremia - manifestations of uremia (confusion, bleeding, pericarditis)
122
Q

Management of post-renal AKI?

A
  • Watch drugs, fluid balance, lytes, acid-base, and uremia.
  • Drugs – SADMAN to hold: Sulfonylurea/SGLT2i, ACEi, Diuretics, Metformin, ARB, NSAIDs
  • Fluid balance – most patients with this lose ability to regulate volume status, thus cannot dilute/concentrate urine or excrete a proper amount of urine/sodium. Need to regulate intake or overload will occur! Maintenance fluids (100-125 mL/hr) usually with RL
  • Lytes – problems can occur with K, Na, Ca, PO4, Mg. Major issue is HYPERKALEMIA >5.3
    • stabilize myocardium (calcium Cl/gluconate 10ml of 10%). Ca increases threshold for action potential
    • shift K+ (insulin IV w/ D50W (glucose), B agonist)
    • Remove K+, watch drugs/intake = loop diuretics (Lasix)
    • Everyone K >6 should order an ECG – peaked T waves, widened QRS
  • Uremia – syndrome due to accumulation of waste products form protein catabolism. Can lead to azotemia = increase in nitrogenous waste in blood.
123
Q

Clinical features of ATN?

A

Typically presents as an abrupt rise in urea and Cr after a hypotensive episode, sepsis, rhabdomyolysis, or administration of nephrotoxic drug

124
Q

What is AIN?

A

Acute inflammatory cell infltrates into renal interstitium

125
Q

Etiology for AIN?

A

Hypersensitivity

    1. antibiotics: β-lactams, sulfonamides, rifampin, quinolones, cephalosporins, fluoroquinolones
    1. other: NSAIDs, allopurinol, furosemide, thiazides, triamterene, PPIs, acyclovir, phenytoin, cimetidine

Infections
- Bacterial pyelonephritis, Streptococcus, brucellosis, Legionella, CMV, EBV, toxoplasmosis, leptospirosis, HIV, Mycoplasma

Immune: SLE, acute allogra rejection, Sjögren’s syndrome, sarcoidosis, mixed essential cryoglobulinemia

Idiopathic (renal-ocular syndrome – acute tubulointerstitial nephritis plus uveitis)

126
Q

Urine and blood findings for AIN?

A

Urine

  • mild, non-nephrotic range proteinuria (<1g/d protein) and microscopic hematuria
  • sterile pyuria, WBC casts
  • eosinophils if AIN

Blood work

  • increased Cr and urea
  • eosinophilia if drug reaction (high negative predictive value, common in β-lactam reactions)
  • normal AG metabolic acidosis (RTA)
  • hypophosphatemia, hypo- OR hyperkalemia, hyponatremia
127
Q

Renal biopsy findings for AIN?

A

Renal biopsy definitive – shows interstitial infiltrates and edema on biopsy sparing glomeruli and blood vessels

128
Q

Treatment for AIN?

A
  • Treat underlying cause (e.g. stop offending medications, antibiotics if pyelonephritis)
  • Corticosteroids (may be indicated in allergic or immune disease)
129
Q

Pathophysiology of Anti-GBM antibody–mediated?

A

Circulating antibodies directed against a-3-chain of Type 4 collagen, intrinsic to GBM and alveolar BM. Results in small vessel inflammation.

130
Q

Presentation of Anti-GBM antibody–mediated?

A

Viral prodrome absent. Renal involvement, sometimes pulm involvement, no systemic

131
Q

Types of Anti-GBM antibody–mediated?

A
  • Anti-GBM GN (without lung hemorrhage*)

- Goodpasture syndrome (with lung hemorrhage)

132
Q

Investigations for Anti-GBM antibody–mediated?

A

Anti GBM Ab titres, ANCA

133
Q

Treatment fpr Anti-GBM antibody–mediated?

A

Initial- steroids + cyclophosphamide (OR Rituximab) + plasma exchanger. Treat ASAP or ESKD!!!

134
Q

Pathophysiology for ANCA-associated vasculitis?

A

Circulating antibodies directed against neutrophil antigens in cytoplasm. Results in small vessel inflammation.

135
Q

Types of ANCA-associated vasculitis?

A

1) Microscopic PA
2) Granulomacytosis PA
3) Eosinophilic Granulomatosis PA

136
Q

Presentation for ANCA-associated vasculitis?

A

1) MPA- mainly renal
2) GPA- renal, pulm, ENT, & systemic
3) EGPA- asthma, some renal

137
Q

Causes of ANCA-associated vasculitis?

A

Causes: Granulomatosis with polyangiitis, Microscopic polyangiitis

138
Q

Investigations for ANCA-associated vasculitis?

A

ANCA

139
Q

Treatment for ANCA-associated vasculitis?

A
  • Initial- steroids + cyclophosphamide (OR Rituximab)
  • Maintenance- Azathioprine OR Rituximab
  • Treat ASAP or ESKD!!!

LMCC (anglais) (23 decks)

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