Nephrology Flashcards
Name a few causes of low vs. high BUN
High
- high protein diet
- antianabolic meds (steroids, tetracyclines)
- catabolic process (fever, infection)
- low effective arterial blood volume
- UGIB
Low
- low protein diet
- malnutrition
- impaired hepatic function
What is the expected rise in serum creatinine in 24h-period in average patient with anuric AKI? When can it be expected to be worse?
- 88-176mmol/L per day
- extreme catabolic state, rhabdo
Risk factors for developing AKI?
- prior CKD
- age
- diabetes
- black race
What are the symptoms of AKI?
- Asymptomatic
- Decreased urine output
- Peripheral edema
- Gross hematuria
- SOB
- Uremia symptoms: fatigue, weak, N/V, low appetite, pruritus, asterixis, paresthesia, anemia, pericarditis
When should you consider RRT in patients with AKI?
- anuria >6h
- severe oliguria (<200ml x12h)
- severe hyperK (>6.5)
- severe metabolic acidosis (pH<7.2 with normal PaCO2)
- hypervolemia (esp. if pulm. edema present)
- severe azotemia
- uremia sequelae (eg., pericarditis)
Definition of CKD?
- presence of kidney damage (albuminuria), or
- decreased kidney function (GFR <60) >3 months
Structures affected in AKI:
1. prerenal
2. intrarenal
3. postrenal
- structures: up to and including afferent arterioles
- renal parenchyma: glomeruli, interstitium, tubules, blood vessels
- any: process obstructing urine flow
Biocemical lab to suggest prerenal AKI? Intrarenal?
BUN:creat
- pre: >20:1 (caused by increased urea reabsorption in PCT 2/2 low effective arterial blood volume
- intra: <15:1
FENa
- pre: <1% or <35% (if on diuretics)
- intra: >1-2% or >35%
Urine sediments:
- prerenal
- intrarenal
- postrenal
Prerenal
- Bland, hyaline casts
Intrarenal
- ATN: granular, “muddy”, pigmented; tubular epithelial cells
- AIN: WBC casts
- GN: RBC casts
- Nephrotic: Fatty casts
Postrenal
- Hematuria (stones, bladder Ca, clots)
- Absent (neurogenic bladder)
How does hyperCa2+ cause AKI?
Causes:
- a reduction in glomerular filtration related to afferent arteriolar contriction
- renal salt wasting –> hypovolemia
HRS 1 vs 2: main difference?
HRS 1
- Rapid, doubling creatinine in <2wks
- commonly associated with MOF
- Oliguria more common
HRS 2
- Indolent
- Stable course often associated with refractory ascites
What are the general categories of intrarenal AKI?
- Vascular
- GN
- ATN
- AIN
Which type of vasculitis can involve the renal artery? Associated with intrarenal AKI?
Renal Artery
- Medium: PAN, Kawasaki
- Large: GCA, Takaysu
Intrarenal AKI
- Small: GPA, eGPA, Churg-Strauss Syndrome, microscopic polyangiitis, HSP (often cause GN)
What are the lab features of atheroembolic renal disease? (intrarenal AKI)
- peripheral + urinary eosinophilia
- serum hypocomplementation
- other labs can indicate other organ involvement: hepatocellular injury (etc.)
What is the mechanism of AKI in ATN?
Tubular dysfunction 2/2 tubular epithelial cell injury (ischemic vs. toxic)
What is the timing + prognosis of contrast-induced nephropathy?
- CIN develops 24-48h after contrast exposure
- Recovery usually within 7-10 days
Common meds associated with ATN?
- NSAIDS
- Vancomycin
- Aminoglycosides
- Polymyxins
- Pentamidine
- Ampho B
- Foscarnet
- Tenofovir
- Cisplatin
- MTX
Why pigment and contrast-induced nephropathies can sometimes be associated with FENa <1%?
In addition to toxicity of renal tubules, they can induce afferent arteriole constriction = prerenal physiology
What is AIN? Classic triad?
- Inflammation + edema within renal interstitium
- Triad: fever, maculopapular rash, peripheral eosinophilia (all 3 present only 10-15% of cases)
Meds associated with AIN?
Most common:
- NSAID + antibiotics
- PCN, cephalosporins, cipro, rifampin, sulfa, vanco
Others:
- Allopurinol, acyclovir, famotidine, lasix, PPI, phenytoin
When does AIN usually develop in relation to exposure to medication?
- 7-10 days
- sooner possible, especially if repeat exposure to culprit drug
AIN etiology typically meds, infection, autoimmune, and tubulointerstitial nephritis uveitis (rare). Which infection more commonly associated with AIN? Autoimmune? Which population typically affected by TINU?
Infection
- bacterial: brucella, campylobacter, e. coli, legionella, salmonella, strep, staphy, yersinia
- viral: CMV, EBV, HIV, hantavirus
Autoimmune
- SLE, sarcoidosis, sjorgren
TINU
- young women
- S&S: uveitis, TIN, constitutional symptoms
Which malignancies are typically associated with renal obstruction?
- RCC
- bladder
- prostate
- TCC of collecting system
- MM
- mets
Most common primary cause of glomerular disease?
IgA Nephropathy
Nephrotic vs Nephritic syndromes: urinary findings
Nephrotic
- proteinuria >3.5g/d
- fatty casts: frothy urine
- microscopic hematuria
- sediment: bland
Nephritic
- sediment: dysmorphic RBC, RBC casts +/- WBC
- varying proteinuria <3.5g/d
- hematuria
- sterile pyuria
DDx: Nephrotic vs. Nephritic; BONUS - most common causes of nephritic-nephrotic syndrome?
Nephrotic
- MCD
- FSGS
- Membranous nephropathy
- Diabetes
- Amyloi light chain, amyloidosis, light chain deposition
- Lupus nephritis
Nephritic
- PSGN
- IgA nephropathy (Berger)
- GPA, eGPA (Wegener)
- Goodpasture
- Alport
- RPGN
- Lupus nephritis
Nephritic-nephrotic syndrome
- Membranoproliferative GN
- Diffuse proliferative GN
Nephrotic syndrome: what are the [1] symptoms, [2] exam findings?
Symptoms
- swelling, weight gain (nephrotic)
- fatigue
- dyspnea
- foamy urine
Exam
- HTN
- peripheral edema
- ascites
- pleural effusions
- less common: Muehrcke’s lines [nails], eruptive xanthoma, xanthelesma
General lab features of nephrotic syndrome?
- proteinuria >3.5g/d
- albumin <2.5g/dL
- hyperlipidemia
- creatinine variable
Common sites of theombosis in nephrotic syndrome?
- renal veins
- lower extremity veins
Agents available to treat nephrotic syndrome?
ACEi
Which primary cause of nephrotic syndrome associated with thromboembolism more?
membranous nephropathy
Meds associated with nephrotic syndrome?
- NSAIDs
- lithium
- gold
- penicillamine
- captopril
- tamoxifen
What infections are associated with nephrotic syndrome?
- Bacterial: IE, vDRL
- Viral: HIVm HBV, HCV
- Protozoal: malaria, toxoplasmosis
- Helminthic: schistosomiasis, filariasis
Most common malignancies associated with nephrotic syndrome?
- MM
- lymphoma
- lung
- RCC
In addition to amyloidosis as secondary cause of nephrotic syndrome, what other disease associated with fibrillar deposits in mesangium or GBM?
- fibrillary GN (more common)
- immunotactoid glomerulopathy
Nephritic syndrome: symptoms and exam findings?
Symptoms
- hematuria, oliguria (AKI)
- CP, dyspnea (uremic pericarditis)
- peripheral edema (low albumin)
- headache (HTN)
Exam
- HTN
- Skin: palpable purpura (small-vessel vasculitis)
- pericardial friction rub (uremic pericarditis)
What type of dysmorphic RBC is most specific for GN?
Acanthocytes, ring-shaped RBCs with vesicle-shaped protrusions (“mickey Mouse ears”)
What are the subcategories of GN based on serology?
- ANCA+
- Anti-GBM+
- Low C3/4
- Other
What does “ANCA” refer to?
Antineutrophil cytoplasmic antibodies: group of antibodies against proteins found in the cytoplasm of neutrophils (eg., PR3, MPO)
When patients are ANCA positive, what are the 2 distinct patterns seen on immunofluorescence microscopy?
- c-ANCA: antibodies to PR3
- p-ANCA: antibodies to MPO
What causes of GN are associated with low complement levels?
- PSGN (low c3, normal c4)
- Membranoproliferative GN (low c3, normal c4)
- SLE (both low, but C3<C4)
- IE (low c3, normal c4)
- Cryoglobulinemia (low C4 ++, N-low C3)
DDx of renal injury in the setting of IE?
- renal infarction 2/2 septic emboli
- AIN 2/2 meds
- ATN 2/2 septicemia or abx
Typical clinical features of IgA nephropathy? % of which will progress to ESRD?
Typically 2nd/3rd decades
More common white/asian men
2 presentations:
1. macroscopic hematuria usually ~5 days s/p URTI (more common in <40yo), or
2. asymptomatic with abn urine sediment + proteinuria (more common in older)
40%!!!
What 2 causes of GN are histologically the same? How are the differentiated?
- HSP and IgA nephropathy
- Extrarenal manifestations: palpable purpura is universally present in HSP
Symptoms of hyperK+?
- cardiac arrhythmia, palpitations
- weakness, paralysis, paresthesia
- N/V, diarrhea
- reduced DTR
ECG changes of hyperK+?
What [1] conduction abnormalities and [2] dysrhythmias are assocaited with hyperK+?
Conduction
- BBB
- bifascicular block
- AV block
Dysrhythmia
- sinus brady
- asystole
- idioventricular rhythms (VT, VF)
DDx: Hematuria (4 main categories)
1) Pigments
- beets, myoglobin, hemoglobin, porphyrin, rifampin, food colouring
2) Transient:
- menstruation, UTI, fever, exercise, trauma, endometriosis, renal vein thrombosis
3) Glomerular
- nephritic: MPGN II, RPGN, IgA
- hereditary: Alport’s, thin BM disease, Loin pain hematuria syndrome
4) Extra-glomerular
- tumor: kidneys, ureter, bladder, urethra
- stones
- cystic kidney disease: PCKD, medullary cystic kidney disease, medullary sponge kidney
Hematuria: glomerular vs. extra-glomerular
Glomerular
- cola urine
- proteinuria
- dysmorphic RBC (acanthocytes)
- RBC casts
- no clots
Extra-glomerular
- bright red urine
- no proteinuria
- no dysmorphic RBC, clots, RBC casts
DDx: Proteinuria (4 main categories)
1) Functional [<1g/d]
- infection, fever, exercise, orthostatic
2) Tubular [0.5-1g/d]
- interstitial nephritis, ATN
3) Glomerular [1-3g/d, usually >3g/d]
- nephrotic/nephritic syndrome, early diabetes
4) Overflow [any amount, usually >1g/d]
- MM
Proteinuria: test which detects all proteins?
Sulfosalicylic acid test
Which medication can cause “pseudo-renal failure”?
Cimetidine, trimethoprim
- can reduce tubular secretion of creatinine causing small but significant increase in creat w/o change in GFR
Contrast-Induced Nephropathy:
- Timing: onset, peak, recovery
- Risk factors
- Prevention
Timing
- immediately after exposure
- peaks: 48-72h
- recovery: same as ATN
Risk Factors
- CKD, MM, Dm, HTN, volume deplete, HF, nephrotoxins, procedures (dye load)
Prevention
- use low-dose dye (if possible)
- IVF:
1. NS0.45% 1ml/kg/h 12h before/after dye, or
2. NS or NaHCO3 at 3ml/kg/h 1h prior/6h post dye, or
3. NAC 150mg/kg in 500mL NS 30min before contrast then 50mg/kg 4h after
GN terms:
- Focal
- Diffuse
- Segmental
- Global
Area of glomerulus affected:
- Focal: <50%
- Diffuse: >50%
- Segmental: segment of glomerulus
- Global: entire glomerulus
GN: proliferative vs. non-proliferative
Non-proliferative
- lack of cell proliferation in glomerulus, usually nephrotic
Proliferative
- increased cells # in glomerulus; usually nephritic
DDx: non-proliferative vs. proliferative GN
Non-Proliferative (nephrotic)
- MCD
- FSGS
- Membranous
- Other (amyloidosis/MGRS, Dm)
Proliferative (nephritic)
- MPGN
- ANCA: GPA, eGPA
- RPGN (linear, immune, pauci immune)
Causes (primary/secondary) of Nephrotic syndromes?
1) MCD
- Cancer: T-cell lymphoma/Hodgkins, leukemias
- Drugs: NSAIDs, Li, COX2i
- Infx (rare): HIV, EBV, TB
2) FSGS (more severe form of MCD)
- Drugs: Li, heroin, pamidronate, ‘roids
- Hyperfiltration: obesity, single kidney, reflux nephropathy, HTN, SCD
- Infx: HIV, parvo, EBV
3) Membranous
- SLE
- Cancer: solid tumors, CLL
- Drugs: gold, penacillamine, NSAID, anti-TNFs
- Infx: HBV, HCV, HIV, syphilis
DDx + Tx: RPGN:
1) linear
2) immune
3) pauci immune
1) Linear
- anti-GBM disease (syndrome if lung involved)
- Tx: PLEX + pulse steroids + Cyclo; if no improvement at 3 months, taper off
2) Immune
- SLE: low C3/4; hydroxychloroquine + steroids
- PSGN: low C3; resolves 3-4 weeks
- IgA: normal C3/4; ACEi + steroids + Cyclo/Azathio
- MPGN: low C3/4 - HCV, cryo, CLL) ; steroids + Cyclo
3) Pauci Immune
- ANCA: GPA/Wegener (c-anca), microscopic polyangiitis, eGPA (p-anca), churg-strauss; steroids + Cyclo (if RPGS, if not, use Ritux)
DDx - CKD
- any causes of acute AKI
- renovascular: atherosclerosis, HTN, glomerulosclerosis (with age)
- diabetes
- GNs
- PCKD
- MM
- nephrotoxins
Risk factors for progression of CKD?
- hypertension
- age
- proteinuria
- dyslipidemia
- high protein diet (unclear)
S&S Uremia
- Constitutional: tired, weak
- Neuro: poor concentration, slow speech, myotonic jerks, altered taste/smell, restless leg
- GI: N/V, anorexia
- Heme: anemia, platelets dysfunction
- MSK: bone disorders, cramps
- Derm: pruritus
- Sex: amenorrhea, sex dysfunction
CKD-MBD - targets for PO4, Ca2+, PTH?
- Ca2+: normal
- PO4: <1.5mmol/L
- PTH: <2-3x normal
Criteria for dialysis in CKD?
- any acute (AEIOU) indications
- GFR <10
- albumin <35
- uremic symptoms
How do ACEi help in CKD? Should be started in which patients? When should it be discontinued?
Benefits
- ACEi cause efferent arteriole vasodilation > decrease intraglomerular pressure > decreased long term remodeling/stress > slow progression of CKD
- lowers BP, proteinuria, and mediators of glomerular tubule hypertrophy/fibrosis
Should START
- in all CKD +/- HTN +/- proteinuria
Shoudl STOP
- if >30% rise in creatinine after starting
RTA type I, II, IV (III extremely rare)
- Patho
- Serum K+
- Serum HCO3
- Urine pH
- Urine AG (urine net charge; UNC)
- Tx
