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Clinical Medicine 3 > Lecture 14 (Renal)-Exam 5 > Flashcards

Lecture 14 (Renal)-Exam 5 Flashcards

1
Q

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

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
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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?

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
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3
Q
A
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4
Q

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

A
  • Asymptomatic in early stages, symptoms develop as GFR declines
  • HTN is most common sign, see signs of fluid overload
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5
Q

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

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
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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?

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
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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?

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
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8
Q

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

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.
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9
Q

Labs of CKD?
* What do labs ALWAYS show?

A
  • Increased BUN, creatinine, potassium, phosphate, magnesium
  • Decreased bicarb (metabolic acidosis with increased anion gap), calcium, Hgb
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10
Q

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

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

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
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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?

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
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13
Q

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

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
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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?

A
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15
Q

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

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%
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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?

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
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17
Q

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

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
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18
Q

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

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
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19
Q

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

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
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20
Q

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

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”
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21
Q

Renal Osteodystrophy
* What is the txt?(4)

A

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

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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?

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.
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23
Q

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

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

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
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25
Q

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

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
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26
Q

Dietary Management of CKD
* Restrict what? (4)

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
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27
Q

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

A
  • Adjust doses of meds excreted by kidney
  • Restrict laxatives and antacids
  • Restrict NSAIDS
  • Watch morphine – metabolites can accumulate
  • Watch IV contrast
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28
Q

He said low yield so I placed it on one slide

What vaccines do CKD need to have?

A
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29
Q

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

A
  • GFR <15; in actuality5-10 mL/min/1.73m2
  • Requires hemodialysis, peritoneal dialysis or kidney transplant to sustain life
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30
Q

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

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

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31
Q

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

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

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32
Q

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

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

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33
Q

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

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)
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34
Q

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

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
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35
Q

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

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

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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?

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

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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?

A
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38
Q

When do you admit for CKD?

A
  • initiation of dialysis if patient not stable enough for outpatient
  • Patient with worsening acid-base status, electrolyte abnormalities and volume overload
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39
Q

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

A
  • Common with missed dialysis sessions
  • Frequently presents with HTN emergency
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40
Q

Pulmonary Edema in ESRD
* What is the txt?

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)
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41
Q

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

A
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42
Q

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

A
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43
Q

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

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
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44
Q

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

A

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

Physical Exam:
* Refractory ascites, evidence of portal hypertension

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45
Q

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

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
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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?

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?
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47
Q

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

A
  • Oliguria only observed in AKI
  • May have normal to large kidneys
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48
Q

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

A
  • Anemia suggests CKD
  • Small kidney size on US
  • May have normal to large kidneys in early disease
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49
Q

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

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
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50
Q

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

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
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51
Q

Three stages… of AKI
* What is stage 3?

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

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52
Q

Need to know

What is the rifle criteria?

A
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53
Q

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

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
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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?

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
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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?

A
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56
Q

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

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.
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57
Q

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

A
  • Hypocalcemia may occur = long QT segment
  • Hyperphosphatemia may occur
  • Anemia due to erythropoietin production
  • Platelet dysfunction
58
Q

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

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
59
Q
A
60
Q

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

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
61
Q

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

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

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?

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.
63
Q

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

A
  • Urine sodium <20
  • High specific gravity of urine > 1.030
  • Increased urine osmolality > 400-500 mOsm/kg
  • TX – replace volume
64
Q

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

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
65
Q

Post-renal Clinical clues
* What are some clues?
* What are on exam?

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
66
Q

Postrenal AKI (Obstructive Uropathy)
* There is something what? What does this cause?
* How do you dx it?

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

67
Q

Postrenal AKI (Obstructive Uropathy)
* What can the BUN:Cr ratio be (2)
* What imaging do you do?
* What is the tx?

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
68
Q

Diagnosis of Azotemia can be made bywhat?

A

BUN greater than 21 mg/dL

69
Q

Significant Findings for Pre-Renal Azotemia
* BUN:Cr
* FeNA:
* Urine osmo:
* UA:

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
70
Q

Intra-Renal Azotemia
* BUN:Cr
* FeNA:
* Urine osmo:
* UA:

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
71
Q

Post-Renal Azotemia
* BUN:Cr
* FeNA:
* Urine osmo:
* UA:
* What does imaging show?

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
72
Q

Labs on postrenal AKI
* What are the initally? What does it look like?
* After a few days what is present?

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
73
Q

Labs of post renal AKI
* What is isosthenuria
* Kidneys have lost the ability to do what?

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
74
Q

Diagnostic Studies & Treatment of post renal
* Bladder cath and ultrasonography to assess for what?
* If cause not determined by US, then do what?
* How do you tx?

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
75
Q

Referral and Admission for AKI
* When do you need to refer to nephro?
* When do you need to refer to urologist?
* Admit all patients with what?

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
76
Q

What are the three types of intrinsic kindey injury? What is the BUN/CR ratio?

A
  • Acute Interstitial Nephritis
  • Acute Tubular Necrosis
  • Acute Glomerulonephritis
  • Normal BUN/CR ratio: 10-15:1
77
Q

Acute Interstitial Nephritis
* What it is?
* Spares what?
* What is the MCC?

A
  • Inflammatory or allergic response in the interstitium
  • Spares the glomeruli
  • Most common cause – Drug Hypersensitivity ~70%
78
Q

Acute Interstitial Nephritis
* What are the drug culprits?
* What are other causes?

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
79
Q

Acute Interstitial Nephritis
* What are the sxs?
* UA will show what?
* What is the tx?
* What is the recovery?
* How will the kidney function be?

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
80
Q

Acute tubular necrosis
* What is it?
* What are the two ways it can happen?
* If due to prerenal azotemia – often presents as what?

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
81
Q

Acute Tubular Necrosis (ATN)
* What are the exogenous nephrotoxins?
* What are the Endogenous nephrotoxins?

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

82
Q

DX and TX - ATN
* What does the UA show?
* What is lost?
* What is low? (2)

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

83
Q

DX and TX - ATN
* What happens to FENA?
* What about urine Na?
* What is the BUN:Cr ratio?

A
  • Increased FENA > 2%
  • Increased urine sodium >40 meq/L
  • BUN: creatinine ration < 15:1
84
Q

DX and TX - ATN
* What is the managment?

A

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

85
Q

Contrast-Induced Renal Failure
* What is a common complication of contrast administration, occurring 1-2 days after admin?
* High-risk patients should be what?
* Who has a higher risk?
* What/when do sx occur?

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
86
Q

Contrast-Induced Renal Failure
* What is the prevention?

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

87
Q

Acute Glomerulonephritis
* What are causes? (2)
* IgA nephropathy called what?

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
88
Q

Acute Glomerulonephritis
* What is Membranoproliferative/Mesangiocapillary?
* What is rapidly progressive glomerulonephrits?
* What is the prognosis of rapid/progessive?

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
89
Q
  • Acute nephritic syndrome is what?
  • What is Nephritic syndromeandacute glomerulonephritis?
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.
90
Q

Acute Glomerulonephritis
* What is the classic sign?
* What are other sxs?

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)
91
Q

Acute Glomerulonephritis
* What is going on with the UA?
* Increase what?
* What can be proformed and what does it show?

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)
92
Q

AGN TX
* What is the outcome?
* What do you give for IgA nephropathy?

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
93
Q

AGN TX
* What do you do for the edema, HTN and hypervolemia?
* What do you do for strep?
* What do you do for Rapid/progressive or severe disease ?

A
  • Edema, HTN, hypervolemia – Loop diuretics, beta-blockers, CCBs
  • Post strep AGN- maybe antibiotics
  • Rapid/progressive or severe disease – Corticosteroids plus Cyclophosphamide
94
Q
A
95
Q

Nephrotic Syndrome
* Glomerular damage leads to what?
* How do you dx it? (4)
* What is shown clinically?

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
96
Q

Nephrotic syndrome:
* What are the causes? (general)

A
  • Minimal Change disease or Nil disease
  • DM
  • Focal segment glomeruosclerosis
  • Membranous nephropathy
97
Q

Nephrotic syndrome
* Minimal change disease or nil disease: Mc in who? What causes proteinuria?
* Membranous nephropathy: MC in who? Causes?

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
98
Q

Nephrotic syndrome: “Focal segment glomerulosclerosis”
* Causes? (3)
* MC in who?
* Stems from what?
* What is the hallmark of histo?

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

99
Q

Nephrotic Syndrome
* How is this a minimal change disease?
* What is shown on polarized light mircoscopy?

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
100
Q

Nephrotic Hallmark Features
* Urine protein?
* Albumin?
* Cholesterol?
* What happens to water?
* What type of state?

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)

101
Q

Nephrotic Syndrome DX, TX
* how do you Dx it? (3)
* What does the UA show?
* Need to measure protein via what?
* What is going on with lipids and albumin?

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
102
Q

Nephrotic Syndrome
* What is a diagnostic clue to membranous nephropathy?
* How do you tx it?

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
103
Q

Nephritic syndrome
* What some causes? (5)

A
104
Q

Nephritic Syndrome
* What is it? What happens to urine protein and RBC?
* What are clues?
* What do you see clinically?

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
105
Q

Nephritic Syndrome
* What happens to in the urine?
* Less extra, more benign, when severe it is termed what?

A
  • Proteinuria <3.5 g/day, hematuria, RBC casts
  • termed rapidly progressive glomerulonephritis
106
Q

Common Clinical Manifestations
* What are the sxs of nephritic syndrome? (4)

A
  • Mild edema
  • Moderate proteinuria
  • HTN: Always causes HTN
  • Hematuria (brown or “smoky”) & RBC casts
107
Q

How do you dx nephritic syndrome?

A
108
Q

how do you txt nephritic syndrome?

A
109
Q

Wegener’s Granulomatosis
* What is it?
* What is positve for dx? What else can you do?

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
110
Q

Wegener’s Granulomatosis
* What are the clinical features?
* Prognosis? What is the txt?

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

111
Q

Goodpasture’s Syndrome
* Falls within what?
* What type of response?
* What is positive?

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
112
Q

Goodpasture’s Syndrome
* What are the sxs?
* What does the CXR show?
* What is going on with kidney?
* What is the txt?

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

113
Q

Hemolytic-Uremic Syndrome
* A form of what? What does that cause?
* Classic childhood HUS is preceded by what?
* What are the clinical features?

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
114
Q

Hemolytic-Uremic Syndrome
* What do the labs show?
* how do you dx?
* What is the txt?

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)
115
Q

Henoch-Schönlein Purpura
* What is it?
* What is seen in children?
* Seen higher when?
* How do you dx it

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
116
Q

Henoch-Schönlein Purpura
* What is present?
* What is seen on biopsy of skin lesions?
* What is going on with urine?
* What is the txt?

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

117
Q

Hereditary Nephritis (Alport’s Syndrome)
* More common in who?
* What happens by age 30?
* What does biopsy show?

A
  • M>F(sex linked)
  • Renal failure usually develops by age 30
  • Biopsy shows thinned and thickened capillary loops with splitting of GBM
118
Q

Hereditary Nephritis (Alport’s Syndrome)
* Usually presents when? With what?
* Txt?
* Common where?
* high associatation with what?

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
119
Q

Nephrotic vs. Nephritis
* The hallmark features of the nephrotic syndrome include:
* Common features of the nephritic syndrome are:

A
120
Q

A note regarding Vascular
* Know there are both what?
* Know that anything that impacts Systemic vascular system also impacts what?
* What occurs?

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
121
Q

Renal Vascular Disease
* Renal vasculature is unusually complex with what?
* What commonly threatens the blood supply of the kidney?
* The glomerular capillary endothelium shares susceptibility to what?
* Changes in blood supply are followed by?

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
122
Q

Renal Vascular Hypertension (Renal Artery Stenosis)
* Suspect under the following circumstances (6)

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
123
Q

Renal Vascular Hypertension (Intrinsic)
* MCC of what?
* HTN due to what?
* What is the pahtophysiology?
* What are the causes?

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

124
Q

Clinical – Renovascular HTN
* Suspect it in pts with what?
* Suspect if when? (HTN)
* If AKI occurs when?
* What is on exam?

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)
125
Q

Renovascular HTN
* What is done outpatient for r/o?
* What is gold standard for dx?

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)

126
Q

TX->Renovascular HTN
* What is the medical txt but contraindicated in who?
* May require adding what?

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).
127
Q

AKI Dx PEARLS
* When should US happen?
* Kidney size may help distinguish between what?
* Kidney biopsy should be considered in patients with what?

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
128
Q

AKI Dx PEARLS
* AKI can be divided into what?
* Tx may require what?
* Find what quickly?

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!!!
129
Q

Renal Cancer:
* What are the risk?
* Majority are what?
* What is usually present?

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
130
Q

Renal Cancer
* What will the CT show?
* Most are what?

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
131
Q

Renal Cell Carcinoma
* Tumor of what?
* These cells are what?
* Renal cell tumor are by far what?
* Difficult to dx, why?
* Once, dx then why is it difficult to treat?

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
132
Q

Renal Cell Carcinoma
* Gender?
* Uncommon dx in what ages?
* Peak incidence whem
* What are thought to be risk factors?
* What are there rare forms of?
* MC form?

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
133
Q

Clinical Presentation of renal cancer:
* What is present in urine?
* Pain?
* What can be felt?
* What are some other sx?

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)
134
Q

Clinical Presentation of renal cancer:
* Typically found as what/
* What is common?

A
  • Typically found as an incidental finding on x-ray
  • Hypercalcemia is common
135
Q

Dx work up of renal cancer
* What do you need to get done? (4)

A
  • Urinalysis
  • Urine cytology
  • CT scan of abdomen and pelvis
  • Chest radiograph – get a CT if anything suspicious on CXR
136
Q

What are Other renal presenting neoplasms? (4)

A
  • Transitional cell carcinoma of the renal pelvis
  • Sarcoma
  • Lymphoma
  • Wilms’ tumor
137
Q

Treatment & Staging of renal cancer
* What is txt if no metastasis?
* What if metastasis?
* What is the survival rate?

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)
138
Q
A
139
Q

Wilms Tumor/Nephroblastoma
* MC in who?
* MCC of what?
* May be accompanied by what?

A
  • Most common in children under 5 years old
  • Most common cause of abdominal mass in children
  • May be accompanied by GU abnormalities
140
Q

Wilms Tumor/Nephroblastoma
* What are the sxs?
* How do you DX?
* What other area do you need to check?
* ~10% will have what?

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
141
Q

Wilms Tumor/Nephroblastoma
* Treatmetn begins with what??
* What happens with the tumor?
* Therapy is tailored to what?
* TX ?

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.

142
Q
A

Clinical Medicine 3 (27 decks)

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