AKI, CKD Flashcards

(82 cards)

1
Q

KDIGO AKI GUIDELINE

stage 1

stage 2

stage 3

A

•Preferred definition for AKI based on 3 stages consisting of ONLY Cr and Urine Output

•Stage 1

  • Increase Cr 1.5-1.9 baseline or
  • decreased UO

•Stage 2

  • Increase Cr 2-2.9X baseline or
  • UO 12 hrs

•Stage 3

  • Increase Cr 3X baseline or
  • Cr >4 or UO reduction 24hrs or anuria >12hrs
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2
Q

FeNa VS FeUrea or FeUA

A

FeNa: not accurate if pt is on diuretics w/in 24hrs

•FeNa < 1% = pre-renal azotemia

•FeNa >1% = intrinsic renal failure

•FeNa >4% = post-renal failure

FeUA: NOT influenced by diuretics

•FEUrea < 35% or FEUA < 9-10 % = prerenal

•FEUrea > 50% or FEUA > 10-12 % = ATN

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3
Q
  • FeNa < 1% =
  • FeNa >1% =
  • FeNa >4% =
A
  • FeNa < 1% = pre-renal azotemia
  • FeNa >1% = intrinsic renal failure
  • FeNa >4% = post-renal failure
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4
Q

Prerenal inury causes?

A

Hypovolemia

↓ cardiac output

↓ effective circulating volume

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5
Q

Prerenal Injury labs

Volume depletion

Decreased CO/Effective arterial volume

Urine output

A

Volume depletion

Hemoconcentration: ↑ H/H, albumin, calcium

•↑ Na, BUN, Cr

Decreased CO/Effective arterial volume

•Edema

•↓ Na, Albumin

Urine output

•Oliguria (<500ml/d) or anuria (<100ml/day)**

  • High specific gravity (>1.015)
  • Normal sediment or hyaline casts
  • Low Urine Na (<20mEq/L)
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6
Q

tx prerenal dz due to DEC CO effectivenes

A

↓ CO/Effective circulating volume

Optimize cardiac performance carefully

  • •Diuretics (volume overloaded) -high dose IV
  • •Nitrates
  • •Dobutamine
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7
Q

3 categores of intersitial AKI

A

Glomerular

  • PSG
  • IgA Nephropathy
  • Nephrotic syndrome /Minimal change
  • Polycystic kidney Dz

Tubules & Interstitium

  • Acute Tubular Necrosis
  • Acute Interstitial Nephropathy

Vascular

  • Renal Artery Obstruction – vasculitis
  • Renal Vein obstruction
  • Microangiopathy – TTP, HUS, DIC
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8
Q

si/sx of Vascular intersitial AKI

A

FeNa >1% intrinsic renal failure

LE rash: livedo reticularis

urine eosinophils

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9
Q

postrenal AKI can be defined as

A

↑BUN and Cr from obstruction to urine flow in ureters, bladder or urethra (anuric & <5% of ARF

  • BOO (ex. BPH, prostate cancer)
  • Neurogenic bladder
  • Malignancy (ex. ovarian, cervical, retroperitoneal)
  • Pregnancy

Meds (Acyclovir, methotrexate, sulfa drugs

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10
Q

Polycystic Kidney Dz etiology

A

Autosomal dominant genetic disorder

  • cyst formation
  • enlargement of the kidney (and other organs ie. Pancreas, liver, spleen)
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11
Q

si/sx Polycystic Kidney Dz

A

Diffuse pain -abdomen, flank, back

  • •Enlargement of cysts
  • •Hemorrhage into cyst or perinephric hematoma
  • •Infectious – UTI, pyelonephritis, abscess, infected cyst
  • •Nephrolithiasis (20-30%)

HTN

+/- palpable flank mass

+/- hepatomegaly

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12
Q

Tx Polycystic Kidney Dz

A

BP management (ex. ACEI/ARB) =slow progression of dz

Pain management: AVOID NSAIDs

Nephrectomy / Surgical cyst decompression

Monitor & manage recurrent infections: UTI/Cysts

Hematuria: may need transfusion!!!

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13
Q

definition and causes of Acute Interstitial Nephritis

A

allergic reaction to medication

  • Antibiotics: B-lactams, sulfonamides, vancomycin, erythromycin, rifampin
  • •Acyclovir
  • •NSAIDS (either direct toxicity or allergy)
  • •Anticonvulsants: Phenytoin, valproate, carbamazepine

Post-infectious

Autoimmune

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14
Q

si/sx of Acute Interstitial Nephritis

A

After recent new drug exposure

Fever

Skin rash

Peripheral eosinophilia

Oliguria

more commonly, patients are found incidentally to have rising serum creatinine after initiation of new med

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15
Q

WBC casts & Hematuria

Dz?

Tx

A

Acute Interstitial Nephritis

D/c of offending agent: reversal of renal injury

Glucocorticoid therapy: accelerate renal recovery

  • •6 week taper prednisone or
  • •IV methylprednisolone pulse 3 days)
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16
Q

Potential Nephrotoxins that cause ATN

A
  • NSAIDs
  • Chemotherapeutic agents
  • Aminoglycosides
  • Amphotericin
  • Vancomycin
  • Radiocontrast dye (GFR 30 rad cutoff)
  • Poison (ethylene glycol, heavy metals)
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17
Q

UA - Pigmented granular casts (muddy-brown casts)

electrolyte changes?

A

Acute Tubular Necrosis (ATN

Serum hyperkalemia

Serum hyperphosphatemia

Serum hyperuricemia

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18
Q

Tx Acute Tubular Necrosis (ATN

A

Aggressive volume replacement– hydrate (If nephrotoxic agent, volume depletion)

Oliguria present and extracellular-volume normalized:

  • • consider loop-diuretic high dose (100-200mg Lasix) to improve urine output

Protein restriction

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19
Q

Cola colored urine (blood degraded/hematuria/RBC casts)

Edema

Hypertension (salt & fluid retention)

Dx

A

Post-strep glomerulonephritis

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20
Q

dx Post-strep glomerulonephritis

A

+ throat, skin culture for strep A

•Elevated titers of abs to strep products

•(+) Anti-streptolysin (ASO)*

UA: Hematuria – RBC casts

•Proteinuria

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21
Q

(-) strep A antibody test

Urine red or coca cola 1-2 days s/p onset

Dx & Tx

A

IgA Nephropathy

ACE-/ARB, Steroids

Dialysis

Renal transplant

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22
Q

Heavy proteinuria (>3.5g/24hr)

Hypoalbuminemia (<3 g/dL)

Peripheral edema

A

Nephrotic Syndrome: adult

minimal change: children

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23
Q

dx minimal chanhe histology?

A

Light microscopy is normal on renal bx

Histology - diffuse effacement of the epithelial cell foot processes on electron microscopy

Hypoalbuminemia

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24
Q

tx minimal change

A

Prednisone

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25
name uurine sediment that correlated w/ dz
26
define CKD
Progressive loss of renal function that persists for more than 3 months Commonly irreversible Usually caused by long-term diseases such as DM, HTN
27
pathophys of CKD
1. 1.Underlying etiology causes _Adaptive hyperfiltration_ and nephron damage 2. 2.In response to any damage the kidney - kidney ↑ filtration rate to normal undamaged nephrons (_Hyperfiltration_) 3. 3.Hyperfiltration over time = glomerular hypertrophy, distortion of the glomerular architecture, sclerosis and l_oss of remaining nephrons_ 4. 4.Manifested by _proteinuria_ and progressive renal failure
28
RAAS and AII impact on CKD
_RAAS and AII activated trying to maintain GFR_ w/ resultant hyperfiltration however… _↑ Pore size_ in GM by AII = _increasing protein leak_ across the glomerular basement membrane Consequence of repeated and continued activation of the RAAS = _Microalbuminuria/Proteinuria -_ toxic to the tubules
29
define azotemia and how it rekates to uremic syndrome
**Uremic Syndrom**e: clinical manifestations of uremia / advanced renal failure (stage 5) * Symptomatic manifestations associated with Azotemia **Azotemia** = the accumulation of urea and other nitrogenous compounds and toxins caused by the decline in renal function
30
# define CKD stages Stage 1 Stage 2 Stage 3 Stage 4 Stage 5
Stage 1: GFR ≥ 90 Stage 2: GFR 60-89 Stage 3: GFR 30-59 Stage 4: GFR 15-29 Stage 5: GFR \<15 or dialysis
31
CKD maging modality of choice
Renal US (consider other imaging) – imaging modality of choice
32
CKD When to Refer to Nephrology?
* GFR \< 30ml/min (CKD Stages 4 and 5) * Rapidly progressive CKD * Poorly controlled HTN despite 4 agents * Rare or genetic causes Suspected renal artery stenosis
33
si/sx stage 4 CKD
**•Difficult to control HTN: large dose loop diuretics** * Difficult to control edema * Hyperkalemia * Uremia
34
labs in CKD
↑ BUN , Creatinine Hyperkalemia, & phosphatemia Hypocalcemia Proteinuria – RBC/ & WBC cast in urine
35
causes of ESRD leading cause?
DM - leading Cause\*\* Diabetic Nephropathy HTN HTN Nephropathy
36
DM pathophys in CKD
1. Damages vessels in the kidney 2. Elevated blood glucose rises beyond kidneys capacity to reabsorb glucose 3. Glucose remains concentrated in the fluid, raising its osmotic pressure and causing more water to be carried out, increasing urine volume = prerenal hypovolemia and RAAS activation
37
DM Tx
_Primary prevention_ * Tight glucose control * Diet/exercise **•\*BP control \<130/80 - delays the onset of microalbuminuria**
38
Diabetic nephropathy ## Footnote First sign – Most common co-morbidity –
First sign – microalbuminuria Most common co-morbidity –hypertension
39
tx diabteic nephrop
**ACEI/ARB’s – ALL patients even if normotensive** * •renal protective qualities – inhibits angiotensin * •If need another BP lowering med Loop Diuretic – + a second agent to aide in BP control _fluid overload_ avoid sodium Smoking cessation & Protein restriction Treat c_hronic metabolic acidosi_s w/ bicarbonate
40
CKD is a risk factor for _____ disease
CKD is a risk factor for cardiovascular disease
41
Second leading cause of ESRD
**HTN** accelerates the progression of CKD Controlling BP slows down ↓GFR •Inhibiting RAAS is effective in lowering BP and ↓ microalbuminuria
42
HTN Nephropathy is defined as
proteinuria and hypertension
43
tx HTN Nephropathy
**CKD Stages 1-3 w/ proteinuria**: _ACEI/ARB_ * ↓ progression of CKD & ↓ mortality/morbidity in HF _ACEI_: _Monitor serum creatinine & potassium_ concentration * •prior to initiation * •within 2 weeks of starting the drug * •and within 2 weeks after an increases in dose **Stage 4 & 5** require nephron consult before initiating ACEI/ARB
44
when initating an ACEI it is important to monitor? tiumeline?
Monitor **serum creatinine & potassium** concentration * •prior to initiation * •within 2 weeks of starting the drug * •and within 2 weeks after an increases in dose
45
what changes do we expect to see in pt when initiating ACEI? whendo we d/c?
**•Expect worsening creatinine or ↓ GFR** - * if values stabilized after initial rise - continue * (if they do not stabilize d/c & consult nephro) •Contribution to **hyperkalemia, \>6.0mmol/**L - stop any other harmful drugs, ↓ or hold potassium retaining diuretics, ↓ loop diuretic dosage
46
Lowering BP Goals in a patient with CKD and HTN =
\<130/80
47
Most common primary malignant renal tumor in childhood
Wilms Tumor Arises from primitive metanephric blastema: Sporadic or hereditary •Genetics: loss of function mutations of tumor suppression & transcription genes à WT1 suppression gene, Chrom 11
48
Wilms tumor Associated Disorders
GU: cryptorchidism, hypospadias Isolated hemihypertrophy Sporadic aniridia u 10% assoc w/ _congenital malformation syndromes:_ **WAGR:** * •Wilms tumor * •Aniridia * •GU abnormalities * •Retardation, Intellectual disability Beckwith-Wiedeman syndrome Denys-Drash syndrome
49
most common si/sx of wilms tumor
asymptomatic abdominal mass (gentle Wilms tumor are fragile) * Smooth & firm * Well demarcated * Rarely crosses midline
50
imaging for wilms tumor
**Abdominal U/S w/ Doppler:** * Confirms mass arises from kidney * Evaluates contra- kidney * Doppler **Contrast CT for ALL renal tumors:** •Chest, Abdomen– pelvis CT: metastases evaluation
51
tx wilms tumor low risk w/ unitumor most pts high risk
**Radical nephrectomy & LN sampling** _Depending on staging/risk stratification:_ **Very low risk pts w/ uni- tumor**= * Nephrectomy _w/out chemo-/radiation_ **Most pts:** Nephrectomy & _Chemo-_ **High risk pts:** Nephrectomy & _Chemo- & Radiation_
52
staging wilms tumor 1-5
Stage I – tumor limited to Kidney and is completely excised Stage II – Tumor extends beyond the kidney but is completely excised Stage III – Residual tumor confined to the abdomen Stage IV – presence of metastases Stage V – Bilateral renal involvement at the time of diagnosis
53
Renal Artery Stenosis caused by pathophys
**Atherosclerotic diseas**e - ostial & proximal renal arterial segments * More common, elderly, CV risk factors **Fibromuscular dysplasia** -middle & distal renal arterial segments * Younger pts \<50, more common in females _Pathophys:_ 1. Narrowing of renal arteries 2. Kidney hypoperfusion 3. Renovascular hypertension & ischemic nephropathy 4. Renal failure
54
most common si/sxs w/ renal artery stenosis is?
**HTN** * •Onset of HTN 50 y \<30y or \>50 y * •Severe or Refractory HTN * •Resistance to antihypertensive therapy * •Moderate-Severe HTN in pts w/ recurrent episodes of flash Pulmonary edema * •Nο FHx of HTN
55
renal a. stenosis Imaging gold standard
Renal angiography •Done after positive screening test
56
tx Renal Artery Stenosis Atherosclerotic disease s Fibromuscular dysplasia
**Atherosclerotic Disease: Goals:** Control BP, Stabilize renal function, ↓ CV complications _Medical therapy : 1st line: ACEIor ARBs_ * •Monitor Cre, GRF for first wks à If ⬆ Cre: D/C * •Suggests bi- RAS, RAS in Uni- functional kidney, or RAS in allograft if kidney transplant recipient _Angioplasty +/- stenting_ _Surgical bypass_ **Fibromuscular Dysplasia**: Medical therapy alone usually not advised _Percutaneous transluminal angioplasty_: Often curative
57
types of kisney stones common causes
**calcium stones** (Ca oxalate \> Ca phosphate) 15% **struvite** (magnesium ammonium phosphate) * •Uncommon UTI organisms 5% **uric acid** – radiolucent (cannot see on CT) * •Gout, hyperuricosuria 1-3% **cystine**: radiolucent (usu faintly radio-opaque)
58
Si/ Sx Nephrolithiasis
Renal colic begins suddenly & waxes and wanes lasting 20-60 mins Severe unilateral flank pain-- radiating to groin/testicle/labia (T10-S4 dermatome) Pacing, Rocking, Writhing, Constant movement unable to find position of comfort (contrast to peritonitis)
59
dx of choice for stones what do we see on this modality
**NCCT of abdomen + pelvis:** identifies all stone types in all location (uric acid, pure cystine and certain drug stones not seen) * Ureteral dilatation * Collecting system dilatation * Perinephric stranding * Periureteric stranding * Nephromegaly * “Rim sign”
60
imaging modality uses for stones ## Footnote KUB: IVP: US:
**KUB:** NOT radiolucent stones **IVP:** info about the stone * •size, location, radiodensity * •and degree of obstruction. **US**: Detects indirect signs of obstruction: * •Procedure of choice for patients who should avoid radiation * • children, pregnant women and woman in childbearing age.
61
Stone imaging of choice for patients who should avoid radiation
US •children, pregnant women and woman in childbearing age.
62
first line analgesic w/ stones
NSAID ketorolac FIRST LINE)
63
meds for d/c pts w/ stones
give _strainer_ and bring in stone for analysis _Cocktail of medications_ * Diclofenac 50mg po bid * Valium 2mg po QID prn * Tamsulosin 10mg qd * Oxycodone 5-10mg q4-6hr prn
64
defien Staghorn Calculi most common pathogen?
Upper urinary tract stones involve the renal pelvis and extend into at least 2 calyces (struvite stone) * •Always assoc w/ infection - Urease-producing bacteria * •Pro_teus species (most common)_ * •Staphylococcus species, Klebsiella species, Providencia species, and Pseudomonas species
65
dx & Tx Staghorn Calculi:
Rarely present as colic type stones, **no pain!!** _•Medical tx not enough_ - Suppressive antibiotic therapy or Urease inhibitors (acetohydroxamic acid) **•PNL surgical tx of choice** followed by PNL & ESWL combination
66
Med Expulsion Therapy for stones
Tamsulosin – Med Expulsion Therapy •assoc 65% greater likelihood passage \>5mm distal stones
67
imaging study for hydronephrosis & renal stones
US
68
Surgical Options for Stones
Extracorporeal shock wave lithotripsy Ureteroscopy Percutaneous nephrostolithotomy Percutaneous Nephrostomy Open nephrostomy
69
Indications for Surgery of stones CI??
Uncomplicated stone \<10mm not passed in 4-6 wks * Symptomatic stones w/o other etiology for pain * \>10mm stones * Pregnancy and failed observation * Pediatric and failed MET _Contraindications:_ * Active UTI untreated * Coagulopathy * Pregnancy
70
tx of choice in pts w/ stones who ned FAST decompression ## Footnote * Septic or hemodynamically unstable * Significant comorbidity * Stone unlikely to be able to be bypassed with stent
Percutaneous Nephrostomy: Small tube through flank into renal pelvis for decompression (FASTEST) •Bridge to surgery
71
surgical options for stones: ## Footnote proximal stones mid and distal ureteral stones stones \>2cm and proximal collecting system
p**roximal stones**: Extracorporeal shock wave lithotripsy **mid and distal ureteral stones:** Ureteroscopy s**tones \>2cm and proximal collecting system:** Percutaneous nephrostolithotomy
72
most common si/sx Bladder Cancer
Painless Hematuria (80-90%) \*\*
73
types of bladder cancer RF??
**Transitional cell carcinoma** : 90% of bladder Ca * Can arise anywhere in the urinary tract, including the renal pelvis, ureter, bladder, and urethra **Squamous cell carcinoma**: Up to 7% **Adenocarcinoma**: Rare _Risk Factors:_ **Cigarette smoking\*\*** Chronic urinary inflammation (SC injury & chronic catheter) **Occupational exposures\*\*** à organic chemicals, rubber, paint, paper production, and dye industries have increased risks of urothelial cancers.
74
bladder cancer dx standard
Cystoscopy: Diagnostic standard w/ bx
75
tx of bladder cancer ## Footnote Non-muscle invasive Muscle-Invasive disease (
**Non-muscle invasive** (Ta,T1,CIS): _Endoscopic TURBT_ w/ electrocautery or laser fulguration _Radical cystectomy_ _Immunotherapy and chemotherapy_: Intravesical instillation of BCG (Bacillus-Calmette Guerin) vaccine **Muscle-Invasive disease** (T2 and Greater) _Neoadjuvant chemotherapy before radical cystectomy_ (MVAC) * Methotrexate • Vincristine • Adriamycin • Cisplatin _Radical cystectomy w/ regional LN dissection_: Tx of choice\*\*\*\*\*\*\* _Radiation therapy (T2-3)_
76
Renal Cell Carcinoma most common si/sx
**Hematuria (+/-painless)** Weight loss, Fever, Night sweats, Malaise L sided varicocele à obstruction of the testicular v. Supraclavicular LN **CLASSIC TRIAD** 1. flank pain 2. Hematuria 3. flank mass (10%)
77
RCC occurs frquently w/
Frequent occurrence w/ paraneoplastic syndromes
78
RCC diagnostic method of choice
CT w/ contrast :
79
Tx RCC Localized dz Locally advanced dz disseminated
**Localized** dz: neohrectomy T1a \<4cm - partial nephrectomy T1b-T2 radical nephrectomy (recurrent 2-3%) **Locally advanced dz**: venous tumor thrombus à Dx w/ MRI Radical nephrectomy, LN dissection & IVC thrombectomy **disseminated** Palliative radical nephrectomy: to relieve sx Chemo & Radiation therapy: chemo & radioresistant tumor Biologic response modifiers: IL-2 & Interferon alpha Multikinase-inhibitor, VEGF inhibitor treatment
80
Indications of venous tumor thrombus
* lower extremity edema * isolated right-sided varicocele or one that does not collapse with recumbency * dilated superficial abdominal veins * pulmonary embolism * right atrial mass * nonfunction of the involved kidney
81
Bladder Cancer Staging
* TA Noninvasive papillary tumor * Tis Carcinoma in situ flat tumor **•T1** - in wedge _subepithelial conn. tissue_ **•T2** Tumor in _wedge muscle_ * •T2a tumor in superficial m, inner half * •T2b tumor in deep muscle, outer half **•T3:** through the _muscle layer of the bladder & into adipose_ **•T4**: _spread beyond the adipose to nearby organs_ or structures * •T4a: spread to the stroma of the prostate (in men), or uterus /vagina * •T4b: spread to the pelvic or abd wall
82
RCC Staging (1-IV)
**•Stage I:—**Tumor is c_onfined within the kidney_ parenchyma * •**Ia:** \<4cm * •**Ib:** 4-7cm **•Stage II:**—_Tumor (\>7cm) involves the perinephric fat_ but is confined within Gerota's fascia **•Stage IIIA**:—Tumor i_nvolves the main renal vein or inferior vena cava_ **•Stage IIIB:**—Tumor i_nvolves regional LNs_ •**Stage IIIC:**—Tumor involves both _local vessels & regional LNs_ **•Stage IVA:**—Tumor _involves adjacent organs other than the adrenal_ (colon, pancreas, etc). **•Stage IVB:**—_Distant metastases_