Lecture 14 (Renal)-Exam 5 Flashcards

Question 1

Q

CKD
* What is it?
* Evidence of decline may include?
* What are the stages?
* End stage requires what?

Answer

A

This is a progressive decline in renal function
Evidence of decline may include; proteinuria, abnormal urine sediment, decline in GFR, electrolyte disturbance, abnormal urine pH, abnormal urine production
5 major stages based on GFR
End-stage – stage 5 – GFR <15 = uremia requiring dialysis or transplant

Question 2

Q

Chronic Kidney Disease
* What is the single best predictor of disease progression along with decrease in GFR?
* What is the most common two etiology?
* Loow at what for monitoring?

Answer

A

Proteinuria is single best predictor of disease progression along with decrease in GFR
DM most common etiology, HTN second most common
Look at GFR, not Cr for monitoring

Question 3

Q

Question 4

Q

CKD Clinical presentation:
* What are the sxs in early stages? What happens when sxs develops?
* What is the most common sign?

Answer

A

Asymptomatic in early stages, symptoms develop as GFR declines
HTN is most common sign, see signs of fluid overload

Question 5

Q

CKD: What is the dx work up?(5)

Answer

A

H & P
24 hr urine collection= electrolytes and proteins
Renal Biopsy= initritic disease
GFR diagnostic
Urine creatinine to albumin ratio (aka microalbumin)-> help you see changes before GFR changes

Question 6

Q

Urine creatinine to albumin ratio
* What is more predictive of death in the next 10 years?
* Once the ratio goes up, expect what?

Answer

A

Albumin level in urine is more predictive of death in the next 10 years than LDL level.
Once the ratio goes up (>30 -> 300), expect to have CAD events

Question 7

Q

Uremia in CKD
* What are the sxs of Uremia?
* Manifestation of the signs and symptoms of Uremia necessitates what?
* Uremic syndrome is ameliorated with what?

Answer

A

Uremia – nausea, vomiting, fatigue, cramping, easy bruising, dry skin, GI bleeding, fluid overload, malaise, encephalopathy, osteodystrophy (secondary hyperparathyroidism), platelet dysfunction & many more
Manifestation of the signs and symptoms of Uremia necessitates immediate admission and nephrology consult for initiation of dialysis
Uremic syndrome is ameliorated with dialysis

Question 8

Q

Labs of CKD
* What do you use to dx?
* What is the 2nd way to dx?

Answer

A

To diagnose – abnormal GFR persisting for at least 3 months
2nd way to diagnose – persistent proteinuria and abnormalities on renal imaging – even if GFR normal.

Question 9

Q

Labs of CKD?
* What do labs ALWAYS show?

Answer

A

Increased BUN, creatinine, potassium, phosphate, magnesium
Decreased bicarb (metabolic acidosis with increased anion gap), calcium, Hgb

Question 10

Q

Labs of CKD
* What does urinary sediment show?
* What helps narrow down the etiology?

Answer

A

Urinary sediment may show broad waxy casts (early)
Quantify urinary protein – it helps narrow down the etiology

Question 11

Q

Imaging/dx of CKD
* What is shown on US?
* What are large kidneys seen when?
* What may be helpful if inital testing is not clear on etiology?
* _ testing

Answer

A

Small kidneys bilat, <9 cm by US suggest advanced CKD
Large kidneys are seen with polycystic kidney disease, DM nephropathy, HIV nephropathy, plasma cell myeloma, amyloidosis and obstructive uropathy
Kidney Biopsy may be helpful if initial testing is not clear on etiology
Genetic Testing

Question 12

Q

Complications of CKD
* What is associated with more rapid progression of CKD? What does this increase the risk of?
* CKD=
* _
* Why is there an increase risk of Heart failure?

Answer

A

Proteinuria is associated with more rapid progression of CKD and with increased risk of cardiovascular mortality
CKD = more morbidity and mortality from CVD
CAD
Heart Failure – CKD results in greater workload due to hypertension, volume overload and anemia. CKD also causes accelerated rates of atherosclerosis and vascular calcification – lots of left ventricular hypertrophy

Question 13

Q

Complications of CKD
* What does CKD disturb?
* As early as Stage 3 – what can be seen? (3)
* Must control what? How?

Answer

A

CKD disturbs calcium and phosphorus metabolism – making CKD a metabolic bone disease
As early as Stage 3 – hyperphosphatemia, hypocalcemia, hypovitaminosis D = secondary hyperparathyroidism
Must control hyperphosphatemia (can cause gas gangreen) – initially via diet restriction, then via oral phosphorus binders

Question 14

Q

Hematologic complications of CKD
* Anemia do to what? What needs to be supplemented?
* What happens at stage 4,5 (2)
* Why do they have acid-base disorders?

Question 15

Q

Neurologic and endocrine issues with CKD
* What happens with neuro?
* What happens with endocrine?
* What happens with nothers in ESRD and delivery?

Answer

A

Neuro – uremic encephalopathy – occurs when GFR falls below 5-10mL/min/1.73m2. Altered mental status, weakness, asterixis
Endocrine – risk of hypoglycemia, decreased testosterone levels, women can be anovulatory.
Babies born to mothers in ESRD have a mortality rate of nearly 50%

Question 16

Q

Treatment of CKD
* What do you do early in disease?
* What do you give for proteinuria?
* Control what? (2)
* Watch out for what?

Answer

A

HTN – ACE-I or ARBs – do this early in disease!
Proteinuria – same – ACE-I or ARBs – early
Control diabetes if present
Control lipids if hyperlipidemia exists
Watch out for Renal osteodystrophy

Question 17

Q

Treatment of CKD
* Replace what if deficient?
* Dialyses indicated for GFR less than what?
* Avoid what?
* What is last line?

Answer

A

Replace Vit D and calcium if deficient
Dialyses indicated for GFR less than 10ml/min or if serum creatinine 8 or greater, a bit sooner if diabetic.
AVOID nephrotoxic agents!!!
Transplantation

Question 18

Q

Newer Therapies of CKD
* What if there is hyperkalemia associated with CKD?
* Potassium binders (patiromer) can be used to do what?

Answer

A

Usually forces cessation of ACEI/ARB
Potassium binders (patiromer) can be used to reduce K concentration in patient whom still benefit from ACEI/ARB therapy

Question 19

Q

Renal Osteodystrophy
* What is it?
* Decreased what?
* What are the sxs?

Answer

A

Bone disorders often associated with CKD
Decreased renal function in eliminating phosphate + poor synthesis of Vit D
Clinical – muscle aches and pain, bone pain, pathological fractures

Question 20

Q

Renal Osteodystrophy
* How do you dx it?
* What is the imaging?
* May biospy and what will it show?

Answer

A

DX – Hypocalcemia + Hyperphosphatemia + increased parathyroid hormone (PTH). Alk phos may be elevated, Vit D levels vary
Imaging – x-ray may reveal bony cysts, “salt and pepper” appearance of the skull (similar to, but not Paget’s disease – different patho)
May biopsy – may reveal brown hemosiderin material – sometimes called “cystic brown tumor”

Question 21

Q

Renal Osteodystrophy
* What is the txt?(4)

Answer

A

TX – calcium and active forms of Vit D, phosphate binders. PTH lowering meds.

Question 22

Q

Control of Hypertension in CKD
* What can you do nonpharm ways?
* What diuretics can you give in early and late CKD?
* What should you include for protenuric patients? Check what?

Answer

A

Nonpharmacologic – diet, exercise, weight loss, eval and treat obstructive sleep apnea
Diuretics – Thiazides in early CKD, Loop in late
Include ACE inhibitor or ARBs for proteinuric patients – check serum creatinine and potassium within 14 days after initiation or increasing dose. Stop at Cr 3 or greater or if the GFR decreases by 30% with ACEI/ARBs.

Question 23

Q

Control of Hypertension in CKD
* What is the goal BP?
* Do not overtreat what?

Answer

A

Joint National Commission rec re BP – goal of less than 140/90, American Heart Association – less than 130/80
Don’t overtreat HTN

Question 24

Q

Role of ACE-Is and ARBs
* ACEinhibitors effectively reduces what?
* This antihypertensive efficacy probably accounts for an important part of what?
* The reduction in proteinuria appears to be greater when?

Answer

A

ACE inhibitors effectively reduce systemic vascular resistance in patients with hypertension, heartfailure or chronic renal disease
This antihypertensive efficacy probably accounts for an important part of theirlong term renoprotective effects in patients with diabetic and non-diabetic renal disease
The reduction in proteinuria appears to be greater when ACE inhibitors are used in combination with ARBs, although no study has compared combination therapy with doubling the dose of a single agent

Question 25

Q

Role of ACE-Is and ARBs
* However, it has not been proven that what?
* When BP is controlled, what is more effective?

Answer

A

However, it has not been proven that combination therapy improves renal outcomes and adverse effects may be more common
When BP is controlled, renin-angiotensin system (RAS) inhibitors such as ACE-I and ARBs are more effective than other antihypertensive drugs in reducing proteinuria, regardless of the etiology of CKD

Question 26

Q

Dietary Management of CKD
* Restrict what? (4)

Answer

A

Restrict protein to 0.6 – 0.8 g/kg/day
Restrict sodium to 2 g/day
Restrict Potassium once GFR falls below 10-20 mL/min/1.73m2
Restrict Phosphorus to 800-1000mg/day – educate patients regarding level of phosphorus in processed food/colas, eggs, dairy, nuts, beans, meat

Question 27

Q

Medication Management of CKD
* Adjust what?
* Restrict use of what? (2)
* Watch for what? (2)

Answer

A

Adjust doses of meds excreted by kidney
Restrict laxatives and antacids
Restrict NSAIDS
Watch morphine – metabolites can accumulate
Watch IV contrast

Question 28

Q

He said low yield so I placed it on one slide

What vaccines do CKD need to have?

Question 29

Q

End Stage Renal Disease
* What is the GFR?
* Requires what (txt)

Answer

A

GFR <15; in actuality5-10 mL/min/1.73m2
Requires hemodialysis, peritoneal dialysis or kidney transplant to sustain life

Question 30

Q

End Stage Renal Disease
* Refer patient to nephrology when?
* What are dialysis indication (4)

Answer

A

Refer patients to Nephrology in late stage 3 or if GFR declining rapidly

Dialysis Indications:
* Refractory Hyperkalemia
* Metabolic Acidosis
* Volume Overload
* Mental Status Changes

Question 31

Q

End Stage Renal Disease
* Must still ask what? Why?

Answer

A

MUST still ask if patients make urine while on dialysis
* Will affect your decision-making regarding IV contrast or Medications in fluid overload (Lasix)
* Cup of urine= some drugs that will work but NOT contrast
* No urine= use contrast because kidneys are already dead

Question 32

Q

hemodialysis:
* need what access?
* What can be used short term? High risk of what?
* How often does dialysis occur?
* Results is what?

Answer

A

Need vascular access – arteriovenous fistula or prosthetic graft
Indwelling (Quinton) catheter may be used short-term – high risk of infection
Dialysis happens three times a week and lasts 3-5 hours
Result is a state of low dose heparinization (for each session)

Overall lower risk of clotting due to heparinization at each session, so less likely to develop PE

Question 33

Q

A-V Fistula vs A-V Shunt
* Fistula infection rate?
* Survival time?
* How much fluid?
* What is common probelm in fistula?

Answer

A

Fistula Infection rate 1/10 that of a shunt
Survival time 3 times that of a shunt->44% at 10 years
250-300 mL/min can be as high as 600 mL/min
Thrombosis (common problem in fistula)

Question 34

Q

Peritoneal Dialysis
* What is it?
* Water and solutes move how?

Answer

A

Dialysate instilled into the peritoneal cavity through an indwelling catheter
Water and solutes move across the capillary bed that lies between visceral and parietal layers of the membrane into the dialysate

Question 35

Q

Peritoneal Dialysis
* What is Continuous ambulatory peritoneal dialysis (CAPD)
* What is Continuous cyclic peritoneal dialysis (CCPD)?
* Risk of what? Culture what?

Answer

A

Continuous ambulatory peritoneal dialysis (CAPD) – patient exchanges the dialysate a few times per day manually
Continuous cyclic peritoneal dialysis (CCPD) – utilizes a cycler machine to automatically perform exchanges at night
Risk of peritonitis but can be done at home
* Culture all cloudy dialysate fluid + Intraperitoneal ABX

peritonitis: abdominal pain+ dialysis

Question 36

Q

Renal transplant
* 2/3 come from who?
* What is the avg wait time?
* What is the survival rate?
* Offers the best potential for what?

Answer

A

2/3 come from deceased donors
Avg wait is 2-3 years
5-year survival rate of 80% for living donor transplants, 66% for deceased donor transplants
Offers the best potential for complete rehabilitation

> 100,000 on the waiting list in US

Question 37

Q

Shared decision to not treat CKD
* Who should not?
* Clear communication with what?
* If ESRD present and dialysis not begun, what will have?

Question 38

Q

When do you admit for CKD?

Answer

A

initiation of dialysis if patient not stable enough for outpatient
Patient with worsening acid-base status, electrolyte abnormalities and volume overload

Question 39

Q

Pulmonary Edema in ESRD
* Common with what?
* Frequently presents with what?

Answer

A

Common with missed dialysis sessions
Frequently presents with HTN emergency

Question 40

Q

Pulmonary Edema in ESRD
* What is the txt?

Answer

A

IV Nitroglycerin 20-500 micrograms/minute
IV Lasix 3-5 mg/kg (must make at least a cupful of urine per 24hrs)
Hemodialysis (Definitive Tx)

Question 41

Q

Vaccine list for transplant patients:
* Influenze when?
* Pneumoccal when?
* DTap?

Question 42

Q

Vaccine list for transplant patients:
* Hep B when?
* Herpes Zoster when?
* HPV?
* Meningococcal?

Question 43

Q

Hepatorenal syndrome
* What is it?
* Resembles what? But does not respond what?
* Precipitated by what?

Answer

A

Renal failure is patient with severely compromised liver function in the absence of other known causes of renal failure (decreased effective circulating volume)
Resembles prerenal failure (marked renal vasoconstriction) but does not respond to conventional volume replacement
Precipitated by worsening liver failure, sepsis, antibiotics or NSAIDs, diuretics, diarrhea and GI bleeding

Question 44

Q

Hepatorenal Syndrome
* What do the labs show? (2)
* What does the physical exam show? (2)

Answer

A

Laboratory hallmarks:
* High urine osmolality
* Low urine sodium < 10 mEq/L

Physical Exam:
* Refractory ascites, evidence of portal hypertension

Question 45

Q

Hepatorenal Syndrome
* What is the txt?
* Some have what?

Answer

A

No specific treatment, prognosis poor; mortality as high as 95% with established hepatorenal syndrome, usually due to worsening liver failure, infection or hemorrhage.
Some have advocated peritoneovenous shunts (LeVeen or Denver); repeated large-volume paracentesis with IV albumin replacement

Question 46

Q

AKI-Disease Duration
* What is it? Measured by what?
* Retention of these substances are called what?
* CKD is what?
* Management of most kidney related issues depend on 1 big factor is what?

Answer

A

Acute Kidney Injury (AKI) – worsening of kidney function over hours to days – waste product retention – measured by Blood Urea Nitrogen (BUN) and Creatinine
* Retention of these substances is called azotemia.
Chronic Kidney Disease (CKD) – abnormal loss of kidney function over months to years
Management of most kidney related issues depend on 1 big factor: is patient WET-DRY-or NORMAL?

Question 47

Q

AKI
* What is only observed in AKI
* May have what?

Answer

A

Oliguria only observed in AKI
May have normal to large kidneys

Question 48

Q

CKD
* What suggests CKD?
* What is the kidney size?

Answer

A

Anemia suggests CKD
Small kidney size on US
May have normal to large kidneys in early disease

Question 49

Q

Definition of AKI
* What happens to serum creatinine?
* inability to maintain what?
* May be what?
* What is oliguric?

Answer

A

An increase in serum creatinine by 0.3 mg/dL or more in 48 hours Or an increase of 1.5 x the known (or assumed) baseline
Inability to maintain acid-base, fluid and electrolyte imbalance
May be oliguric
“Oliguric” – urine production less than 400-500ml per day or less than 20 ml per hour

Question 50

Q

Three stages… of AKI
* What is stage one and two?

Answer

A

Stage 1 – 1.0 to 1.5 fold increase in creatinine or a decline in urinary output to less than 0.5 ml/kg/h over 6-12 hours
Stage 2 – 2.0 to 2.9 fold increase in serum creatinine or decline in urinary output to less than 0.5 mL/kg/h over 12 hours or longer

Question 51

Q

Three stages… of AKI
* What is stage 3?

Answer

A

Stage 3 – 3 fold increase or greater in serum creatinine, an increase in serum creatinine to greater than 4 or decline in urinary output to less than 0.3 mL/kg/h for 24 hours or longer, anuria for 12 hours or longer or initiation of renal replacement therapy

Question 52

Q

Need to know

What is the rifle criteria?

Question 53

Q

Clinical of AKI
* Most will not display what?
* What is uremia? What are the sxs?
* What may be present?

Answer

A

Most will not display symptoms or signs
“Uremia” is a clinical presentation of azotemia due to build-up of waster products, is a constellation of nonspecific signs and symptoms – nausea, vomiting, malaise, altered sensorium (uremic encephalopathy)
HTN may be present

Question 54

Q

Clinical of AKI
* What can be present? (2)
* What can happen with the heart?
* What can happen to lungs, abdominal and other disorders?
* What can happen if severe?

Answer

A

Pericardial effusion and a pericardial friction rub may be present
Arrhythmias can occur especially with hyperkalemia
May have rales, diffuse abd pain, bleeding disorders
Severe – may have asterixis, confusion, seizures

Question 55

Q

Uremic Encephalopathy
* Acute uremic encephalopathy reverses with what? Subtle cognitive difficulties may persist even when?
* Failure to improve substantially following dialysis should alert what?
* In most cases of dialysis, what is rapid and complete?

Question 56

Q

AKI lab
* What is elevated? (2)
* What happens to potassium? EKG?

Answer

A

Elevated creatinine levels present
BUN may be elevated
KEEP in mind – both of these may be true for CKD as well
Hyperkalemia may be present – if so, ECG may show peaked T waves, PR prolongation and QRS widening.

Question 57

Q

Lab of AKI
* What happens to calcium? EKG?
* What happens to phophate?
* What happens to RBC? why?
* _ dysfunction

Answer

A

Hypocalcemia may occur = long QT segment
Hyperphosphatemia may occur
Anemia due to erythropoietin production
Platelet dysfunction

Question 58

Q

Acute Kidney Injury Classification
* What is pre-renal?
* What is intrinsic?
* What is post renal?
* For all them, what increases?

Answer

A

Pre-renal – it’s all about loss of flow to kidneys (perfusion problem)
Intrinsic/Intrarenal – there’s an issue in the kidney
Post- renal – something is blocking urine
For ALL serum creatinine is up from baseline more than 50%; BUN is up as well
* In pre-renal – BUN is up first

Question 59

Q

Question 60

Q

Prerenal-Poor Perfusion
* This may lead to what?
* What is the primary cause?
* What are other issues that can cause it?

Answer

A

This may lead to Intrinsic if allowed to persist (acute tubular necrosis)
The most common type of AKI
Hypovolemia primary cause – diuretics, GI loss, dehydration, sepsis
Hemorrhage, shock, burns, CHF, low Cardiac output

Question 61

Q

Prerenal-Poor Perfusion
* What are common drugs that can cause it? WHy?

Answer

A

– NSAIDS, IV dye – causing afferent arteriole vasoconstriction, ACE inhibitors (esp in setting of bilateral RAS), ARBs causing efferent arteriole dilation, Hypotension due to CHF, anything causing heart to pump inefficiently

Question 62

Q

Prerenal AKI Labs
* If GFR falls acutely – determine if it is what?
* In pre-renal AKI – BUN:creatinine ratio is what?
* Fractional excretion of sodium (FENa) is what?
* Oliguric patients with intrinsic kidney dysfunction typically have what?
* Lower FENa reliable as predictor of what?

Answer

A

If GFR falls acutely – determine if it’s due to prerenal or intrinsic causes
In pre-renal AKI – BUN:creatinine ratio often exceeds 20:1 (Azotemia)
Fractional excretion of sodium (FENa) – less than 1%.
* Oliguric patients with intrinsic kidney dysfunction typically have a high fractional excretion of sodium – greater than 1-2%
* Lower FENa reliable as predictor of pre-renal AKI, higher not reliable as predictor of intrinsic cause due to variability associated with diuretic use. And – use is limited in nonoliguric pts.

Question 63

Q

Prerenal AKI Labs
* What happens with urine sodium?
* What happens with specific gravity of urine?
* What is urine osmol?
* What is txt?

Answer

A

Urine sodium <20
High specific gravity of urine > 1.030
Increased urine osmolality > 400-500 mOsm/kg
TX – replace volume

Question 64

Q

Post-renal Clinical clues
* May be what?
* Obstruction may ne what?
* What are causes?

Answer

A

May be anuric or polyuric (partial obstruction)
Obstruction may be constant or intermittent
Causes – BPH, tumors, bladder outlet obstruction, b/l ureteral stones or strictures

Answer 56

A

Clues – usually asymptomatic – may notice change in urinary output, may be hypertensive
* Some have back or lower abd pain
On exam – may have enlarged prostate, distended bladder, mass in pelvis

Answer 57

A

There is something obstructing the passage of urine
ALWAYS caused by obstruction-> Hydronephrosis
DX – Creatinine is usually ONLY elevated with bilateral kidney involvement

This is actually quite rare

Answer 58

A

BUN: Creatinine ratio <10:1 ONLY if decreased urea, usually initially >15:1 (mimics pre-renal) then later FeNa >2 and decreased BUN/Cr ratio
Use US or CT (± contrast depending on cause and renal function) to look for stones, hydronephrosis, mass etc.
TX – remove obstruction

Answer 59

A

BUN greater than 21 mg/dL

Answer 60

A

BUN: Cr ratio greater than 20:1
FeNa less than 1, FeUr less than 35%
Ur Osmo 500 mOsm/kg
UA can show hyaline casts

Answer 61

A

BUN: Cr ratio less than 20:1
FeNa greater than 2, FeUr greater than 50%
Ur Osmo less than 300 mOsm/kg
UA: Cellular debris, muddy brown casts red cell casts, eosinophils, + proteinuria

Answer 62

A

BUN: Cr ratio less than 20:1
FeNagreater than 2
Ur Osmo less than 300 mOsm/kg
UA: WBC casts
Imaging findings: pyelonephritis, nephrolithiasis, bladder mass

Answer 63

A

May initially reveal high urine osmolality, low urine sodium, high BUN:creatinine ratio and low FENa
This looks like pre-renal azotemia because extensive intrinsic renal damage has not yet occurred
After few days - urine sodium increases, isosthenuria present

Answer 64

A

Isosthenuria – excreted urine with specific gravity that is equal to that of protein free plasma (~1.008-1.012)
Kidneys have lost ability to concentrate urine

Answer 65

A

Bladder cath and ultrasonography to assess for hydroureter, hydronephrosis, large bladder volume despite inability or lack of sensation to void.
If cause not determined by US – CT or MRI (don’t use gadolinium with a eGFR less than 30mL/min/1.73m2).
TX – treat obstruction – caths, stents, surgical

Answer 66

A

Pt with signs of AKI not reversed over 1-2 weeks without uremia – refer to nephrologist
Pt with signs of persistent urinary tract obstruction – refer to Urologist
Admit all patients with sudden loss of kidney function that cannot be handled quickly in outpatient setting (hyperkalemia, volume overload, uremia) and those who need dialysis or emergent urologic procedures

Answer 67

A

Acute Interstitial Nephritis
Acute Tubular Necrosis
Acute Glomerulonephritis
Normal BUN/CR ratio: 10-15:1

Answer 68

A

Inflammatory or allergic response in the interstitium
Spares the glomeruli
Most common cause – Drug Hypersensitivity ~70%

Answer 69

A

Drug culprits – PCN, Sulfa, Cipro, Cephalosporins, Rifampin, Allopurinol, NSAIDs, APAP
Other causes – infection, autoimmune, and in almost 10% of cases – we never know (idiopathic)

NSAIDs do shunting of blood from cortex to medulla and interfere with urine output
Phenacetin/APAP – phenacetin no longer on market

Answer 70

A

Fever, arthralgias, maculopapular rash, eosinophilia
Urinalysis will show WBC Casts and eosinophilswith proteinuria
TX – remove offending agent
Typically a spontaneous recovery
Normal kidney function typically returns within a year

Answer 71

A

Acute destruction and necrosis of the renal tubules of the nephron
2 ways it happens – exogenous and/or endogenous nephrotoxins or prolonged prerenal azotemia
If due to prerenal azotemia – often present hypotensive and/or hypovolemic

Answer 72

A

Exogenous nephrotoxins – IVdye (immediate), Vancomycin , aminoglycosides, cyclosporine, NSAIDS, Cocaine/PCP intoxication
Endogenous – tumor lysis syndrome, myoglobinuria (rhabdomyolysis), lymphoma, Bence-Jones proteins of Multiple Myeloma, leukemia.

Aminoglycosed cause ARF in 5-25% of patients, drug is not metabolized but excreted by kidney, damaging tubules causing ATN after 8-10 days of therapy

Answer 73

A

Urinalysis - ”Muddy Brown Casts”, epithelial cell casts
Sodium and water reabsorption is lost
Low specific gravity
Low urine osmolarity <500 mOsm/kg

Isostheuria: cannot cont. urine

Answer 74

A

Increased FENA > 2%
Increased urine sodium >40 meq/L
BUN: creatinine ration < 15:1

Answer 75

A

TX – first – IV fluids and remove offending agent(s)

Answer 76

A

ATN is a common complication of contrast administration, occurring 1-2 days after admin
High-risk patients should be kept well hydrated by administration of half-normal saline for 8-12 hours prior to and after procedure
Risk is 40% for patient with diabetes
Oliguria and other symptoms develop in 24 hrs

Answer 77

A

N-acetylcystine 600 mg po bid x 2d (1 before and day of)
* Half-life 5.6-18 hours depending on race
* This is same drug used in Tylenol overdoses

Answer 78

A

Several etiologies – post-infection (think strep) and AUTOIMMUNE (Lupus)
IgA nephropathy called Berger’s Disease - most common cause of Chronic GN in adults. Younger males a day or two post URI or GI illness

Answer 79

A

Membranoproliferative/Mesangiocapillary – SLE, hepatitis – this one has a mixed nephrotic/nephritic presentation
Only 2 present, always, as rapid/progressive - Goodpasture’s disease (anti-GBM disease) and vasculitis
Rapid/progressive – poor prognosis, ESRD in months

Answer 80

A

Acute nephritic syndrome is a group of symptoms that occur with some disorders that cause swelling and inflammation of the glomeruli in the kidney, orglomerulonephritis.
Glomerulonephritisrefers to a number of kidney problems that involve inflammation in the glomeruli, which are the kidney’s filtration units.Acute glomerulonephritiscan causenephritic syndrome.

Answer 81

A

Hematuria – classic sign “tea colored” or “coca cola colored” urine
Edema (peripheral and periorbital) -> HTN is common
Fever, abdominal pain, flank pain, malaise, oliguria (remember this is AKI)
* Lupus rash and other characteristics (ANA; anti-dsDNA)

Answer 82

A

Hematuria, RBC casts, proteinuria, high specific gravity greater than 1.020 osm.
Increased BUN and creatinine
Renal biopsy(IgA deposits in mesangium for IgA nephropathy)

Answer 83

A

All forms except the rapidly progressive forms are typically self-limiting
IgA nephropathy – ACE inhibitors, maybe corticosteroids
* Only transplant shown to be effective therapy, but IgA redeposits ~ 30% in 20yrs

Answer 84

A

Edema, HTN, hypervolemia – Loop diuretics, beta-blockers, CCBs
Post strep AGN- maybe antibiotics
Rapid/progressive or severe disease – Corticosteroids plus Cyclophosphamide

Answer 85

A

Glomerular damage leads to protein loss
Dx – proteinuria, hypoalbuminemia, edema (think osmosis or decreases intravascular oncotic pressure), hyperlipidemia
Clinical – peripheralEDEMA, dyspnea due to pleural effusion, fatty casts in urine, Proteinuria > 3.5g/DAY

Answer 86

A

Minimal Change disease or Nil disease
DM
Focal segment glomeruosclerosis
Membranous nephropathy

Answer 87

A

“Minimal Change Disease” or “Nil Disease” – MCD in children – viral illness, allergies, Hodgkin disease – loss of negative charge of basement membrane causes proteinuria
”Membranous nephropathy” – most common in Caucasian males over 40
* 75% primary, 25% secondary to SLE, hep B, tumors

Answer 88

A

HIV, heroin, HTN
* Most common form of nephrotic syndrome in African American patients
* Stems from abnormalities in the podocyte
* Hallmark of Histology =Podocyte detachment and death lead to the segmental sclerosis

Answer 89

A

Minimal change disease – cannot see under regular microscope, need electron microscope to visualize microscopic damage to base membrane of glomeruli.
* Podocytes arespecialized epithelial cells that cover the outer surfaces of glomerular capillaries.
Oval fat body casts exhibit “Maltese cross” configuration by polarized light microscopy

Answer 90

A

Urine protein > 3500 mg/24hr OR proteinuria >3500 mg (or 4+)-> cause urine to be frothy
HYPOalbuminemia (usually <3.0 g/dL [30g/L])
Hypercholesterolemia
EDEMA (anasarca, ascites)
Hypercoagulable state (loss of anticoagulant proteins)

NO HTN (unless pre-existing)

Answer 91

A

DX: H&P, 24 hr urine, renal bx
UA – “foamy” urine, lipids in urine
Need to measure protein via 24 hour urine which should show > 3.5 g/day
Hyperlipidemia, hypoalbuminemia

Answer 92

A

Diagnostic clue to membranous nephropathy – thick basement membrane on biopsy showing Subepithelial immune deposits of IgG
TX – glucocorticoids (SLE or MCD), loop or thiazide diuretics, ACE or ARB, statin, immunosuppressives
* 90% respond to steroids, 70% relapse and may eventually need cytotoxics

Answer 93

A

Immune-mediated – increased urinary protein and RBC loss
Clues – proteinuria, HTN, azotemia, oliguria, hematuria ->RBC casts
Clinical – HTN, hematuria, less than 400ml per day of urine, fever, abd/flank pain – might have edema

Answer 94

A

Proteinuria <3.5 g/day, hematuria, RBC casts
termed rapidly progressive glomerulonephritis

Answer 95

A

Mild edema
Moderate proteinuria
HTN: Always causes HTN
Hematuria (brown or “smoky”) & RBC casts

Answer 96

A

Small-vessel vasculitis associated with necrotizing granulomatous inflammation affecting the upper and lower respiratory tracts and kidneys
Renal pathology not specific for WG->ANCAs positive in 65-90%
Definitive: biopsy-> large necrotizing granulomas

Answer 97

A

Clinical features: fever, malaise, purpuric rash, pulmonary hemorrhage, sinusitis (septal perforation, saddle nose deformity) & Thrombocytosis-> Triad of URI (nose MC), LRI (lung) and glomerulonephritis

Prognosis poor without treatment (90% mortality 2 years)
* Steroids and cytotoxic agents can produce remission in about 75%
* 11% progress to ESRD

Answer 98

A

Falls within “Rapidly Progressive Glomerulonephritis”
Autoimmune response ( UgG against type IV collagen) and antibody generated directly against glomerular membrane and alveoli
ANCA + in 80%, Anti-glomerular basement membrane antibodies

Answer 99

A

Sxs:
* Pulmonary hemorrhage (cough, hemoptysis, dyspnea) 70%
* CXR: patchy or diffuse alveolar infiltrates
* Renal failure: rapid, oliguric, hematuric with modest proteinuria

Treatment: aimed at reducing circulating preformed anti-GBM antibodies by daily plasma exchange for 14 days, steroids, cytotoxics

Answer 100

A

A form of thrombotic microangiopathy: systemic platelet consumption with formation of intraluminal platelet thrombi
Classic childhood HUS is preceded by an acute diarrheal illness caused by an E. coli strain
Clinical features: renal failure (uremia), mental status changes preceded by 1 week of diarrheal illness

Answer 101

A

Lab: hemolytic anemia with abnormal RBCs (schistocytes – scarred RBC) on peripheral blood smear, low platelet count, increased LDH, increased bilirubin, decreased haptoglobin
Thrombocytopenia with normal coagulation studies
Treatment is supportive (dialysis if necessary)

Answer 102

A

IgA nephropathy associated with systemic vasculitis
Small vessel vasculitis most often seen in children.
Higher incidence in winter and spring
Clincally but coagulation labs are normal, kidney biopsy shows IgA depostis and leujocytoclastic vasculitis

Answer 103

A

Palpable purpuric lesions over buttocks, hematuria, synovial arthritis, abdominal pain (HSP-> Affects IGA so HSPA)
IgA + C3 deposits seen on biopsy of skin lesions
Hematuria, proteinuria, RBC casts, normal C3 levels
Self-limited course normally (supportive Tx), but 10% progress to end-stage renal disease

Henoch-Schönlein Purpura

Answer 104

A

M>F(sex linked)
Renal failure usually develops by age 30
Biopsy shows thinned and thickened capillary loops with splitting of GBM

Answer 105

A

Usually presents in childhood with recurrent gross hematuria, mild proteinuria, nephrotic syndrome is rare
No effective treatment available
Common in East Tennessee
High association with deafness

Answer 106

A

Know there are both microvascular and macrovascular etiologies
Know that anything that impacts systemic vascular system can also impact renal function
Renal artery dissection, renal vein thrombosis occurs, as does embolic disease

Answer 107

A

Renal vasculature is unusually complex with a rich arteriolar flow – basically a filter organ.
Large-vessel atherosclerosis, fibromuscular diseases, and embolic disorders commonly threaten the blood supply of the kidney
The glomerular capillary endothelium shares susceptibility to oxidative stress, pressure injury and inflammation with other vascular territories.
Changes in blood supply are followed by tubulointerstitial fibrosis and loss of kidney function

Answer 108

A

HTN onset before age 20 or after age 50
HTN resistant to 3 or more drugs
You detect epigastric or renal artery bruits
There is atherosclerotic disease of the aorta or peripheral arteries
There is an abrupt increase of more than 25-30% in level of serum creatinine after admin of ACE inhibitors
There are episodes of pulmonary edema associated with abrupt surges in blood pressure

Answer 109

A

most common cause of secondary HTN
HTN due to renal artery stenosis (RAS)
Pathophysiology – decreased renal blood flow leading to activation of the renin-angiotensin-aldosterone system
Causes – atherosclerosis (elderly), fibromuscular dysplasia (women, typically under 50)

Beta blockers reduce renin

Answer 110

A

Suspect it in pts with headache + HTN + less than 20 y/o or over 50 y/o with severe HTN.
If you are unable to get HTN controlled via several drugs.
If AKI occurs after initiation of ACE-I
Exam – Abdominal bruit(rare)

Answer 111

A

Ultrasound – typical test done outpatient to r/o RAS in resistant HTN

Gold standard – revascularization via renal catheter arteriography both diagnoses and treats
* You only order diagnostic imaging if the plan includes treatment intervention (only in severe disease)

Answer 112

A

Medical management – ACE-I or ARBs. BUT – both are contraindicated if bilateral stenosis present or if the patient has only 1 kidney!
May require adding a thiazide diuretic, long-acting CCB or mineralocorticoid receptor antagonist (Aldactone).

Answer 113

A

Ultrasonography of the kidneys and bladder should be obtained for suspected urinary tract obstruction or when the underlying cause of AKI is unclear
Kidney size may help distinguish between AKI and CKD because diminished kidney size and cortical thinning suggest CKD
Kidney biopsy should be considered in patients with AKI from no apparent cause, suspected glomerulonephritis, or unexplained systemic disease

Answer 114

A

AKI can be divided into prerenal, intrinsic, and postrenal causes
Tx may require short-term dialysis (known as RRT – renal replacement therapy)
Find the cause quickly: the kidneys may recover!!!

Answer 115

A

Risks – bladder cancer, Balkan nephropathy, Lynch syndrome, smoking, exposure to radioactive thorium (‘60’s) and who have a long history of analgesic abuse.
Majority are urothelial cell cancers.
Hematuria – gross or microscopic usually present

Answer 116

A

CT will show intraluminal filling defect or nonvisual of collecting system and hydronephrosis
Most are excised, chemo prior to surgery thought to improve outcomes

Answer 117

A

Tumor of the proximal convoluted renal tubule cells
These cells are high metabolically active which increases risk of dysplasia
Renal Cell tumors are by far the most common tumor originating in the kidney (~95%)
Difficult to diagnose due to typically being asymptomatic.
Once diagnosed – difficult to treat – resistant to chemo and radiation

Answer 118

A

Male to Female ratio is 2:1
Uncommon diagnosis in patients under 45
Peak incidence 65-74 years
Cigarette smoking, obesity and hypertensionthought to be risk factors
There are some rare genetic familial forms
MC form – Clear cell RCC

Answer 119

A

Hematuria (May be microscopic and asymptomatic otherwise)
Flank or Abdominal pain
Flank or palpable Abdominal mass
Fever, weight loss, anemia and varicocele (sudden, elderly)

Answer 120

A

Typically found as an incidental finding on x-ray
Hypercalcemia is common

Answer 121

A

Urinalysis
Urine cytology
CT scan of abdomen and pelvis
Chest radiograph – get a CT if anything suspicious on CXR

Answer 122

A

Transitional cell carcinoma of the renal pelvis
Sarcoma
Lymphoma
Wilms’ tumor

Answer 123

A

Surgical if no metastasis
Individualized plan if metastasis present
5 year survival rate ~74% across all stages, goes down of course with later stages (8% in stage IV)

Answer 124

A

Most common in children under 5 years old
Most common cause of abdominal mass in children
May be accompanied by GU abnormalities

Answer 125

A

Clinical – palpable abdominal mass does NOT cross midline, hematuria, nausea, vomiting, HTN, anorexia – may be present. Mass may be only clinically apparent finding
DX – US first, CT with contrast or MRI
Do a CXR – lungs most common site for metastasis.
~10% will have metastasis at time ofdiagnosis

Answer 126

A

Treatment begins with surgical exploration of the abdomen via an anterior surgical approach – allows for inspection and palpation of contralateral kidney
En bloc resection of the tumor.
Therapy is tailored to staging during surgery – need experienced surgeon.
TX – total nephrectomy pluschemotherapy/radiation

En bloc resection involvesthe surgical removal of the entirety of a tumor without violating its capsule, and requires resection of the lesion encased by a continuous margin of healthy tissue.