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Renal II Cumulative Final > CLMD - Hematuria, Proteinuria, AKI > Flashcards

CLMD - Hematuria, Proteinuria, AKI Flashcards

1
Q

Benign causes of hematuria

A

Vigorous exercise

Infection or viral illness

Menstruation

Exposure to trauma

Recent urologic procedure (i.e., catheterization)

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2
Q

Exercise-induced hematuria may also be accompanied by proteinuria and is likely related to decreased RBF, nephron ischemia, increased permeability, and subsequent passage of RBCs. It is particularly common in track athletes and lacrosse players. NSAIDs may also play a role. What are the guidelines for eval and management of these pts?

A

Evaluation: r/o infection

Rest 48-72 hours and recheck

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3
Q

Physiologic effects of NSAIDs on the kidneys

A

NSAIDs may contribute to kidney damage by inhibition of cyclooxygenase within kidney (RL enzyme for prostaglandins that protect kidney by modulating vasoconstriction) — vasoconstriction increased

Ibuprofen decreases GFR compared to placebo or acetaminophen

Indomethacin and celecoxib decrease free water clearance

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4
Q

Urine dipsticks have up to a 35% false positive rate; it is important to obtain a clean catch, mid-stream sample for UA.

What are some potential causes of false positives in terms of hematuria?

A

Myoglobinuria, hemoglobinuria

High alkaline urine (pH > 9) — suggests proteus infection

Ascorbic acid (vit C)

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5
Q

Urine dipstick results can be confirmed with microscopy. How many RBCs can be present to still be considered negative for hematuria?

A

Less than 3 RBC/hpf is negative for hematuria

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6
Q

What are some examples of nonpenetrating kidney trauma that may lead to hematuria?

A

Dorsolateral blunt impact, driving 12th rib into kidney —> rupture [evidence of rib fractures or penetrating trauma raises suspicion for kidney injury]

Kidney driven against lumbar transverse process by blow in flank —> rupture

Tear of renal a. by continued downward momentum of kidney after impact of fall

Rupture of hydronephrotic renal pelvis

Ventral impact may also be transmitted to kidney

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7
Q

T/f: pts with suspected traumatic kidney injury that are hemodynamically stable do NOT require radiographic evaluation

A

True

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8
Q

What type of renal malignancy is associated with Sickle Cell Trait (SCT, HbAS)

A

Renal Medullary Carcinoma (SCT&raquo_space;> SCD)

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9
Q

Describe how Sickle Cell Trait contributes to kidney damage

A

Single hemoglobin S mutation —> impaired urinary concentration

May develop renal papillary necrosis

Hyperfiltration leads to albuminuria, interstitial fibrosis, and decreased number of nephrons (FSGS)

Increased risk of renal medullary carcinoma

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10
Q

Risk factors for transitional cell carcinoma

A

Male

> 35 years old

Current or former tobacco use

Analgesic abuse

Exposure to chemicals or dyes (benzenes or aromatic amines)

Exposure to carcinogenic agents or chemotherapy (alkylating agents)

[other important historical elements: gross hematuria, urologic disorder/disease, irritative voiding symptoms, pelvic irradiation, chronic UTI, chronic indwelling foreign body]

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11
Q

Initial steps in management of pts suspected to have urothelial malignancy

A

Be sure you have complete hx

Always evaluate with culture and sensitivity to r/o infection

Always confirm with microscopy to r/o false positive

Serum evaluation of renal function: BUN, Cr

Radiographic eval: ultrasound vs. CTU (best option)

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12
Q

Compare US to CTU for renal eval

A

US = no radiation, lower cost, very good for tumors >3 cm, cysts, and hydronephrosis — BUT may miss small stones, small bladder masses, and urothelial transitional cell carcinoma

CTU = given with and without contrast, highly sensitive for renal calculi, able to detect small renal parenchymal masses, aneurysm, and renal+perirenal abscesses — BUT higher dose of radiation, exposure to contrast agents, higher cost

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13
Q

The American Urological Association recommends that all patients >35 with asymptomatic microhematuria (or all pts with risk factors for urologic malignancies regardless of age) get a ______

A

Cystoscopy

[note that primary care typically performs after negative US or IVP]

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14
Q

Describe cystoscopy including pros/cons

A

Evaluates bladder via direct visualization

Pros: better assessment of bladder wall for microstructural changes; can identify urethral stricture disease, benign hyperplasia and bladder masses

Cons: invasive, requires sedation, risk of post-procedural UTI

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15
Q

Summary of RAAS effect in terms of vascular/hemodynamic vs. inflammatory

A

Vascular/hemodynamic:
Activation of RAAS leads to vasoconstriction of afferent arterioles (as well as systemic) and efferent arterioles, increases glomerular pressures (hyperfiltration); causes DIRECT glomerular damage

Inflammatory:
Activates inflammatory system and leads to interstitial and tubular fibrosis

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16
Q

How do you clinically determine acute vs. chronic glomerulonephritis

A

Requires detailed history: PMH (genetic d/o, systemic dz like atherosclerosis, HTN, DM), FH (hereditary dz like lupus, sickle cell, autoimmune dz, DM, CAD), recent infections (strep, malaria, schistosomiasis), chronic infectious diseases (HIV, chronic Hep B or C), review of systems (itching, nausea, HA, anorexia, dyspnea, vomiting, diarrhea, hiccup, restlessness, depression)

Review of previous lab data — UA and chemistries

Renal US to assess size of kidneys (generally reduced in chronic dz)

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17
Q

UA findings with glomerulonephritis

A

Always presents with some type of hematuria and proteinuria, often asymptomatic and as few as 3-5 RBC

Red blood cell casts or dysmorphic RBCs found in sediment!!

Gross hematuria present in sickle cell and IgA nephropathy (tea or cola-colored)

18
Q

Lab findings and symptoms in sustained proteinuria vs. benign proteinuria

A

Sustained: >1-2 g/24 hours; symptoms include edema and/or “foamy” urine

Benign/functional/transient: <1-2 g/24 hours; may be related to fever, exercise, obesity, sleep apnea, emotional stress, CHF, orthostatic proteinuria

19
Q

What is the mechanism of damage in hypertensive nephropathy?

A

RAAS and hyperfiltration with subsequent inflammatory changes and fibrosis

20
Q

Epidemiology and risk factors associated with hypertensive nephrosclerosis

A

5x more common in AA than white

APOL1 (functional gene for apolipoprotein 1) expressed in podocyte accounds for increased risk in AA

Other risks: smoking, male, hypercholesterolemia, duration of HTN, low birth weight, preexisting renal injury

21
Q

What are 3 clinical signs of hypertensive nephrosclerosis, and what clinical intervention delays progression to ESRD?

A

Signs include HTN, microhematuria, and moderate proteinuria

Blood pressure control delays progression to ESRD

22
Q

General pathologic changes in diabetic nephropathy

A

Damage related to ECM accumulation in both GBM and tubular basement membrane

Imbalance between synthesis and degradation —> expansion of mesangium

Glomerular filtration surface is decreased by reduced glomerular luminal space which leads to reduction in GFR

23
Q

What are the differences in diabetic nephropathy between type 1 and type 2 diabetics?

A

Type 1 — glomerular, tubular, interstitial, and vascular lesions tend to progress more or less in parallel and independent of albuminuria

Type 2 — variable in progression and can develop albuminuria with little change in the nephron

[Both present clinically stable; edema and worsening HTN are late findings]

24
Q

On routine dipstick, the threshold for a positive result is over ____ mg of albumin

A

300 mg

25
Q

Once protein is identified as positive on urine dipstick, what are the next steps?

A

Quantify the protein using albumin/creatinine ratio (ACR) or using 24 hr urine collection (which also provides sample to do electrophoresis to determine which types of protein)

Other next steps are based on differential dx, derived from thorough hx and PE

26
Q

Nephrotic range proteinuria is NOT the same thing as nephrotic syndrome. In order to be considered nephrotic syndrome, there must be nephrotic range proteinuria along with what other findings?

A

Hyperlipidemia
Hypoalbuminemia
Edema

27
Q

What patient population requires an annual ACR?

A

Pts with established dx of T2DM

28
Q

What drug classes are used to slow the progression of proteinuria?

A

ACE-inhibitors

ARB’s

29
Q

Possible rheumatologic causes of nephrotic syndrome

A

SLE

RA

30
Q

Possible infectious causes for nephrotic syndrome

A

Hep B or C
HIV
Syphilis
Tb

31
Q

Possible hematologic/oncologic causes for nephrotic syndrome

A

Amyloidosis
Multiple myeloma
Sickle cell anemia
Malignancy (liquid and solid tumors)

32
Q

Possible drug-induced causes for nephrotic syndrome

A

NSAIDs
Lithium
IV heroin abuse

33
Q

What factors can alter serum creatinine?

A 
Age
Sex
Race
Muscle mass
Catabolic rate
34
Q

How do you determine acute vs. “acute on chronic” kidney disease?

A

Obtain most recent serum Cr and compare to one 3+ months before acute event

35
Q

Prerenal causes of AKI

A

Hypovolemia

Decreased cardiac output

Decreased ECV (CHF, liver failure)

Impaired renal autoregulation (NSAIDs, ACE-I/ARB, Cyclosporine)

36
Q

Intrinsic causes of AKI

A

Glomerular — acute glomerulonephritis

Tubules and interstitium — ischemia, sepsis, infections, exogenous nephrotoxins (iodinated contrast, aminoglycosides, amphotericin B, PPIs, NSAIDs), endogenous nephrotoxins (hemolysis, rhabdomyolysis, myeloma, intratubular crystals

Vascular — vasculitis, malignant HTN, TTP-HUS

37
Q

Postrenal causes of AKI

A

Bladder outlet obstruction

Bilateral pelvoureteral obstruction (or unilateral obstruction of a solitary functioning kidney)

38
Q

How is the cause of AKI determined clinically (i.e. differentiating between pre, post, and intrinsic cause?)

A

Serum Na and Cr

Urine Na and Cr

Other diagnostics: K+, Cl, CO2, CBC, liver enzymes, Coags

Imaging — US, EKG

39
Q

Treatment of pre-renal AKI

A

Remove/treat underlying contributing factors — stop likely medication offenders like NSAIDs, cyclosporin, etc. — ACUTELY stop ACE-I/ARB

40
Q

Treatment for post-renal AKI

A

Drain urinary bladder — retention catheter or repeat catheterization

Eliminate obstructive process — retrieve/pass stones, reduce size of prostate, ureterostomy or nephrostomy stents to avoid hydronephrosis

41
Q

Treatment for intrinsic AKI

A

Improve renal perfusion — optimize cardiac output, minimize sequestration of circulating volume in 3rd spaces, give IV fluids (NS is preferred but lactated ringers also an option - just watch K+)

Renal II Cumulative Final (20 decks)

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