CLMD - Hematuria, Proteinuria, AKI Flashcards
Benign causes of hematuria
Vigorous exercise
Infection or viral illness
Menstruation
Exposure to trauma
Recent urologic procedure (i.e., catheterization)
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?
Evaluation: r/o infection
Rest 48-72 hours and recheck
Physiologic effects of NSAIDs on the kidneys
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
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?
Myoglobinuria, hemoglobinuria
High alkaline urine (pH > 9) — suggests proteus infection
Ascorbic acid (vit C)
Urine dipstick results can be confirmed with microscopy. How many RBCs can be present to still be considered negative for hematuria?
Less than 3 RBC/hpf is negative for hematuria
What are some examples of nonpenetrating kidney trauma that may lead to hematuria?
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
T/f: pts with suspected traumatic kidney injury that are hemodynamically stable do NOT require radiographic evaluation
True
What type of renal malignancy is associated with Sickle Cell Trait (SCT, HbAS)
Renal Medullary Carcinoma (SCT»_space;> SCD)
Describe how Sickle Cell Trait contributes to kidney damage
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
Risk factors for transitional cell carcinoma
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]
Initial steps in management of pts suspected to have urothelial malignancy
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)
Compare US to CTU for renal eval
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
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 ______
Cystoscopy
[note that primary care typically performs after negative US or IVP]
Describe cystoscopy including pros/cons
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
Summary of RAAS effect in terms of vascular/hemodynamic vs. inflammatory
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
How do you clinically determine acute vs. chronic glomerulonephritis
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)
UA findings with glomerulonephritis
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)
Lab findings and symptoms in sustained proteinuria vs. benign proteinuria
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
What is the mechanism of damage in hypertensive nephropathy?
RAAS and hyperfiltration with subsequent inflammatory changes and fibrosis
Epidemiology and risk factors associated with hypertensive nephrosclerosis
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
What are 3 clinical signs of hypertensive nephrosclerosis, and what clinical intervention delays progression to ESRD?
Signs include HTN, microhematuria, and moderate proteinuria
Blood pressure control delays progression to ESRD
General pathologic changes in diabetic nephropathy
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
What are the differences in diabetic nephropathy between type 1 and type 2 diabetics?
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]
On routine dipstick, the threshold for a positive result is over ____ mg of albumin
300 mg
Once protein is identified as positive on urine dipstick, what are the next steps?
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
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?
Hyperlipidemia
Hypoalbuminemia
Edema
What patient population requires an annual ACR?
Pts with established dx of T2DM
What drug classes are used to slow the progression of proteinuria?
ACE-inhibitors
ARB’s
Possible rheumatologic causes of nephrotic syndrome
SLE
RA
Possible infectious causes for nephrotic syndrome
Hep B or C
HIV
Syphilis
Tb
Possible hematologic/oncologic causes for nephrotic syndrome
Amyloidosis
Multiple myeloma
Sickle cell anemia
Malignancy (liquid and solid tumors)
Possible drug-induced causes for nephrotic syndrome
NSAIDs
Lithium
IV heroin abuse
What factors can alter serum creatinine?
Age Sex Race Muscle mass Catabolic rate
How do you determine acute vs. “acute on chronic” kidney disease?
Obtain most recent serum Cr and compare to one 3+ months before acute event
Prerenal causes of AKI
Hypovolemia
Decreased cardiac output
Decreased ECV (CHF, liver failure)
Impaired renal autoregulation (NSAIDs, ACE-I/ARB, Cyclosporine)
Intrinsic causes of AKI
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
Postrenal causes of AKI
Bladder outlet obstruction
Bilateral pelvoureteral obstruction (or unilateral obstruction of a solitary functioning kidney)
How is the cause of AKI determined clinically (i.e. differentiating between pre, post, and intrinsic cause?)
Serum Na and Cr
Urine Na and Cr
Other diagnostics: K+, Cl, CO2, CBC, liver enzymes, Coags
Imaging — US, EKG
Treatment of pre-renal AKI
Remove/treat underlying contributing factors — stop likely medication offenders like NSAIDs, cyclosporin, etc. — ACUTELY stop ACE-I/ARB
Treatment for post-renal AKI
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
Treatment for intrinsic AKI
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+)
