Azotemia and Urinary Abnormalities – Study Notes (Chapter 55)

Overview

  • Normal kidney functions maintain body homeostasis through many cellular processes; disturbances cause renal abnormalities that present as syndromes.
  • Nephrologic (kidney) syndromes arise from systemic illness or primary renal disease and typically include one or more of:
    • Reduction in glomerular filtration rate (GFR)
    • Abnormal urine sediment (RBCs, WBCs, casts, crystals)
    • Proteinuria (abnormal urinary excretion of serum proteins)
    • Disturbances in urine volume (oliguria, anuria, polyuria)
    • Hypertension and/or edema
    • Electrolyte abnormalities
    • Sometimes fever/pain
  • This chapter focuses on distinguishing renal abnormalities via: (1) reduced GFR, (2) urinary sediment/protein excretion, and (3) urinary volume abnormalities.

Major syndromes and diagnostic clues (Table 55-1)

  • Acute or rapidly progressive renal failure
    • Key clues: Anuria, oliguria, hypertension, hematuria, proteinuria, pyuria, edema; recent decline in GFR; casts.
    • Common label: Acute nephritic syndrome when hematuria with RBC casts is prominent; azotemia with reduced GFR and oliguria.
  • Chronic renal failure (CKD)
    • Azotemia for >3 months; proteinuria and casts; late uremic symptoms; hypocalcemia, hyperphosphatemia, hyperparathyroidism (renal osteodystrophy).
  • Polyuria/nocturia
    • Kidney size reduced bilaterally; edema and hypertension; broad casts in sediment; hyperkalemia and metabolic acidosis.
  • Nephrotic syndrome
    • Proteinuria >3.5 g/24 h per 1.73 m²; casts; hypoalbuminemia; lipiduria; edema; hypercoagulable state; hyperlipidemia.
  • Asymptomatic urinary abnormalities
    • Hematuria; proteinuria below nephrotic range; sterile pyuria; bacteriuria.
  • Urinary tract infection/pyelonephritis
    • Bacteriuria (>10^5 cfu/mL); hematuria; pyuria.
  • Urinary tract obstruction and nephrolithiasis
    • Obstruction signs: azotemia/oliguria/anuria with hematuria and/or pyuria; renal colic; prior stone history; hydronephrosis on imaging.
  • Other tubular/transport defects and electrolyte disorders
    • Polyuria/nocturia; tubular proteinuria (<1 g/24 h); renal calcifications; large kidneys in some conditions; hypomagnesemia and other electrolyte issues; hypertension with proteinuria.

Assessment of GFR and estimation of kidney function

  • Direct measurement of GFR (rare in routine practice):
    • Uses filtered tracer (e.g., inulin or iothalamate) and measures clearance from plasma to urine.
    • GFR = clearance of tracer; units: mL/min.
  • Practical approach: plasma creatinine (PCr) as a surrogate for GFR
    • PCr rises as GFR falls; urine creatinine (UCr) excretion relates to PCr to estimate GFR.
    • In outpatient settings, PCr is used to estimate GFR (less precise).
    • In chronic kidney disease, 1/PCr vs time is roughly linear; slope constant unless superimposed acute process.
    • Uremia signs depend on patient factors; generally symptoms appear when GFR is < ~15 mL/min (GFR < 15 mL/min can reflect advanced renal failure).
  • Azotemia vs uremia
    • Azotemia = elevated nitrogenous waste products due to reduced GFR or perfusion.
    • Uremia = clinical syndrome from renal failure; signs depend on size, age, sex, and underlying disease.
  • Limitations of common markers
    • Urea clearance may underestimate GFR due to tubule reabsorption.
    • Creatinine is produced from muscle; relatively constant daily production but can be influenced by diet (meat intake) and advanced CKD (tubular secretion increases).
  • Direct vs estimated GFR equations (general concepts)
    • CrCl (creatinine clearance) is calculated from timed urine collection:
      CrCl=U<em>extvolimesU</em>extCrP<em>extCrimesT</em>extminCrCl = \frac{U<em>{ ext{vol}} imes U</em>{ ext{Cr}}}{P<em>{ ext{Cr}} imes T</em>{ ext{min}}}
    • Adequacy judged by volume and urinary creatinine content; normal creatinine excretion ranges:
      • For a 20–50 year old man: 18.5–25.0 mg/kg/day
      • For a 20–50 year old woman: 16.5–22.4 mg/kg/day
      • Example: an 80 kg man should excrete ~1500–2000 mg creatinine/day in an adequate collection.
    • Creatinine-based estimates of GFR are widely used but have caveats (diet, muscle mass, timing, catabolic states).
    • eGFR equations developed to estimate GFR using serum creatinine:
    • Cockcroft–Gault (estimates creatinine clearance, not GFR exactly)
    • MDRD (Modification of Diet in Renal Disease) 4-variable formula
    • CKD‑EPI (Chronic Kidney Disease Epidemiology Collaboration) eGFR, often more accurate across GFR ranges
  • CKD-EPI formula (typical representation)
    • eGFR = 141 × min(
      Scr/κ, 1)^{α} × max( Scr/κ, 1)^{-1.209} × 0.993^{Age} × [1.018 if female] × [1.159 if Black]
    • Parameters:
    • Scr = serum creatinine
    • κ = 0.7 for females, 0.9 for males
    • α = −0.329 for females, −0.411 for males
    • Note: Race modifier is controversial; some centers omit the race coefficient due to equity concerns.
  • Other notes on estimation
    • Many calculators exist (e.g., CKD-EPI calculator, MDRD, Cockcroft–Gault).
    • CKD‑EPI with cystatin C and creatinine can improve accuracy; race modifiers are being reconsidered.
    • Limitations: steady-state assumption (no rapid changes in PCr), muscle mass effects, malnutrition, and pregnancy can affect accuracy.
  • Alternative markers and approaches
    • Cystatin C can be less affected by muscle mass and may better detect early GFR decline; combined creatinine-cystatin C equations can improve accuracy.
    • Clinical judgement remains essential; eGFR interpretations should consider context (e.g., bodybuilder with high creatinine due to muscle mass).

Approach to the patient with azotemia

  • Distinguish acute vs chronic renal injury after establishing reduced GFR.
  • Chronic renal failure indicators
    • Anemia, hypocalcemia, hyperphosphatemia, radiographic renal osteodystrophy (late finding).
    • Radiographic evidence of osteodystrophy is a very late sign in ESRD.
  • Role of urinalysis and renal ultrasound
    • Advanced CKD: proteinuria, nonconcentrated urine (isosthenuria), small echogenic kidneys with cortical thinning on ultrasound.
  • Imaging and evaluation strategy
    • Approach figure (Fig. 55-1) highlights steps: assess GFR, determine prerenal vs ATN vs postrenal etiologies, consider tubular/interstitial processes, and use imaging as needed.
  • Management goals
    • Slow progression of renal disease; treat edema, acidosis, anemia, and hyperphosphatemia (discussed in Chap. 322).

Prerenal failure (true hypoperfusion of kidney)

  • Definition and proportion
    • Decreased renal perfusion accounts for 40–80% of acute renal failure and is usually reversible with treatment.
  • Common etiologies
    • Decreased circulating volume: GI bleeding, burns, diarrhea, diuretics.
    • Volume sequestration: pancreatitis, peritonitis, rhabdomyolysis.
    • Decreased effective arterial volume: cardiogenic shock, sepsis.
  • Hemodynamics and renal autoregulation
    • Reduced circulating volume triggers sympathetic activation, renin–angiotensin–aldosterone system (RAAS), and vasopressin (AVP).
    • GFR is maintained via afferent arteriolar dilation (prostaglandins) and efferent arteriolar constriction (angiotensin II).
    • When mean arterial pressure falls below ~80 mmHg, GFR declines steeply.
  • Drug interactions affecting GFR in prerenal states
    • NSAIDs block prostaglandin production, increasing risk of severe vasoconstriction and AKI.
    • ACE inhibitors (ACEi) or ARBs reduce efferent arteriolar tone, lowering glomerular capillary pressure and GFR.
    • Patients with bilateral renal artery stenosis or a solitary kidney depend on efferent arteriolar constriction; ACEi/ARB can precipitously reduce GFR.
  • Progression to ATN
    • Prolonged hypoperfusion can lead to acute tubular necrosis (ATN), an intrinsic renal disease.
  • Distinguishing prerenal azotemia from ATN (urine findings)
    • Prerenal: concentrated urine (>500 mosm/kg), urine Na < 20 mmol/L, FENa < 1%, UCr/PCr > 40.
    • ATN: urine Na > 40 mmol/L, FENa > 2% (though may be <1% in milder/nonoliguric ATN), UCr/PCr < 20.
    • Sediment: prerenal may have hyaline/granular casts; ATN often shows cellular debris, tubular epithelial casts, muddy brown granular casts.
  • Urinary biomarkers for tubular injury
    • Emerging utility in detecting subclinical ATN and clarifying etiology.
  • Postprerenal considerations
    • If obstruction is present, postrenal azotemia should be considered and ruled out early (less than 5% of AKI cases).

Postrenal azotemia (urinary tract obstruction)

  • Definition and prevalence
    • Obstruction accounts for <5% of AKI but is usually reversible.
  • Diagnostic approach
    • Imaging: ultrasound may show ureteral and renal pelvic dilation.
    • If ultrasound is nondiagnostic early, MAG3 renogram or other imaging can help define obstruction.
  • Obligate factors for complete obstruction
    • Requires obstruction at urethra or bladder outlet, bilateral ureteral obstruction, or unilateral obstruction with a single functioning kidney.
  • Management
    • Relieve obstruction; treat underlying cause (urolithiasis, BPH, malignancy, etc.).

Intrinsic renal disease (AKI due to parenchymal disease)

  • Overview
    • When prerenal and postrenal causes are excluded, intrinsic renal disease is diagnosed.
    • Major categories: vascular diseases, intrarenal microvasculature and glomeruli, and tubulointerstitium.
  • Ischemic vs nephrotoxic ATN
    • Ischemic ATN: common after major surgery, trauma, severe hypovolemia, overwhelming sepsis, extensive burns.
    • Nephrotoxic ATN: caused by many drugs/toxins; involves intrarenal vasoconstriction, direct tubule toxicity, and/or tubular obstruction.
  • Drug-induced interstitial nephritis (AIN)
    • Commonly due to antibiotics, NSAIDs, proton pump inhibitors.
    • Urinalysis: mild–moderate proteinuria, hematuria, pyuria (~75%); WBC casts; RBC casts can occur but are not definitive.
    • Urine eosinophils (Wright/Hansel) historically used but not diagnostic; urinary eosinophils lack diagnostic utility for AKI.
    • Renal biopsy often required to distinguish AIN from glomerular diseases.
  • Vascular/other intrinsic etiologies
    • Occlusion of large renal vessels (arteries/veins) is uncommon; bilateral disease or solitary kidney with unilateral occlusion can present with reduced GFR.
    • Atheroembolic renal failure: cholesterol emboli after vascular interventions; eosinophilia and livedo reticularis; may show eosinophils in urine; biopsy often unnecessary if stigmata are present.
    • Renal artery thrombosis/renal vein thrombosis: may present with proteinuria and hematuria; imaging required (angiography).
  • Glomerular and microvascular diseases
    • Present with proteinuria, hematuria, reduced GFR, and sodium handling abnormalities leading to HTN and edema.
    • Presence of RBC casts indicates glomerular disease and prompts early biopsy.
    • Hematuria with RBC casts strongly suggests nephritic processes; RBCs may be dysmorphic in glomerular disease.
    • If RBCs are dysmorphic, phase-contrast microscopy can detect acanthocytes associated with glomerular disease.
    • Common glomerular diseases include IgA nephropathy, hereditary nephritis, thin basement membrane disease; family history often present in hereditary nephritis.
    • Glomerular diseases can present with nephritic or nephrotic syndromes; nephrotic-range proteinuria may occur with various glomerulopathies (not exclusively nephrotic syndromes).

Hematuria, pyuria, and casts: diagnostic approach

  • Isolated hematuria
    • Often indicates urinary tract bleeding; defined as 2–5 RBCs/HPF; dipsticks can be false-positive if no RBCs under microscopy (e.g., myoglobinuria).
    • Common causes: stones, neoplasms, TB, trauma, prostatitis.
    • Gross hematuria with clots suggests postrenal source rather than intrinsic renal disease.
    • Persistent significant microscopic hematuria (>3 RBCs/HPF on three analyses or >100 RBCs in a single urinalysis) warrants investigation for renal/urologic lesions.
  • Glomerular hematuria signs
    • Dysmorphic RBCs and RBC casts with proteinuria (>500 mg/d) are virtually diagnostic of glomerulonephritis.
    • RBC casts form when RBCs enter tubule fluid and get trapped in a gel of Tamm–Horsfall protein.
    • Even without azotemia, serologic evaluation and renal biopsy may be indicated.
  • Pyuria and bacteria
    • Pyuria with bacteria suggests infection (pyelonephritis); treat with antibiotics after cultures.
    • Sterile pyuria (pyuria with negative culture) can occur with urogenital TB or other tubulointerstitial processes.
    • WBC casts and/or WBCs can occur in acute GN and other tubulointerstitial diseases, including transplant rejection.
  • Casts in chronic kidney disease
    • Waxy/broad casts reflect dilated tubules from chronic kidney disease; may appear in the urine.

Abnormalities of urine volume

  • Oliguria and anuria definitions
    • Oliguria: 24-h urine output < 400 mL.
    • Anuria: urine formation < 100 mL/24 h.
  • Causes and implications
    • Anuria can result from complete bilateral urinary tract obstruction, vascular catastrophes (dissection/occlusion), renal vein thrombosis, cast nephropathy, renal cortical necrosis, severe ATN, or severe shock.
    • Oliguria is not normal; it indicates severely reduced kidney function.
    • Nonoliguric AKI: urine output > 400 mL/day with AKI; potassium and hydrogen balance disturbances may be milder; recovery tends to be faster.

Abnormalities of urine protein and nephrotic syndrome

  • Evaluation approach to proteinuria
    • Initiated after a positive dipstick screen; dipsticks primarily detect albumin and can yield false positives with alkaline urine, highly concentrated urine, or contaminated samples.
    • Dilute urine can mask significant proteinuria on dipstick; thus, quantitative assessment is preferred.
  • Albumin-to-creatinine ratio (ACR)
    • Spot urine albumin-to-creatinine ratio approximates 24-h albumin excretion:
    • ACR (mg/g) ≈ AER (mg/24 h).
  • Total protein and protein/creatinine ratio
    • Total urinary protein can be measured by precipitation methods (sulfosalicylic acid or TCA).
    • Protein/creatinine ratio on a spot urine correlates with daily protein excretion; e.g., a ratio of 3.0 roughly equals 3.0 g/day.
  • 24-h urine collection
    • Formal assessment of urinary protein excretion typically requires a 24-h urine protein collection.
  • Pathophysiology and components of proteinuria
    • Normally, glomerular barrier prevents most albumin/globulins; smaller proteins (<20 kDa) are filtered and reabsorbed in proximal tubule.
    • Albuminuria and nonalbumin proteins reflect different mechanisms: glomerular leakage vs tubular or overflow processes.
    • Nephrotic-range proteinuria (>3.5 g/day per 1.73 m²) with hypoalbuminemia, hyperlipidemia, edema may occur.
    • Not all nephrotic-range proteinuria is due to nephrotic syndrome; diabetes can present with heavy proteinuria without classic nephrotic syndrome.
  • Mechanisms of proteinuria by glomerular disease
    • Glomerular barrier selectivity loss leads to albumin-dominant proteinuria (selective vs nonselective):
    • Minimal change disease: selective albumin loss due to foot process effacement.
    • Immune complex diseases: non-selective loss of albumin and other proteins due to basement membrane/slit diaphragm disruption.
    • Filtration barrier components: endothelial pores (~100 nm), glomerular basement membrane, and podocyte slit diaphragms.
    • Proteinuria magnitude and composition depend on the mechanism of injury; higher total protein often indicates nonselective loss.
  • Nephrotic syndrome consequences and pathophysiology
    • Hypoalbuminemia reduces plasma oncotic pressure, causing edema; RAAS activation and AVP increase salt and water reabsorption, promoting edema.
    • Loss of regulatory proteins and hepatic compensation contribute to edema, hyperlipidemia, and hypercoagulability.
    • Loss of antithrombin III and proteins S/C increases thrombotic risk; infections risk rises due to loss of immunoglobulins.
    • Filtered proteases can activate ENaC channels, further promoting Na retention.
  • Common nephrotic-nephritic scenarios
    • Many diseases can cause nephrotic-range proteinuria; nephrotic syndrome can occur with various glomerulopathies as well as with systemic illnesses like diabetes.

Hematuria, pyuria, and casts (detailed approach)

  • Isolated hematuria without proteinuria or casts points to non-glomerular bleeding sources; however, dysmorphic RBCs and RBC casts point to glomerular pathology.
  • Dysmorphic RBCs and RBC casts strongly suggest glomerular disease; phase-contrast microscopy helps detect acanthocytes associated with glomerular bleeding.
  • Pyuria without bacteria can occur in GN or tubulointerstitial disease; sterile pyuria is common in TB and some interstitial processes.
  • Bacteria in urine suggests infection (cystitis, pyelonephritis).
  • RBC casts are highly specific for glomerular disease but not highly sensitive; absence of RBC casts does not rule out glomerulonephritis.
  • In glomerular disease, a biopsy is often warranted to determine specific pathology and guide treatment.

Abnormalities of urine volume: polyuria

  • Distinguishing polyuria from frequency: quantify 24-h urine volume.
  • Polyuria can result from solute diuresis or water diuresis:
    • Solute diuresis: osmolality > 300 mosmol/L and urine volume >3 L/day; caused by elevated solute excretion (e.g., glucose in diabetes mellitus, mannitol, radiocontrast, high-protein intake).
    • Water diuresis: urine osmolality < 250–300 mosmol/L; indicates defects in AVP production or renal responsiveness.
  • Mechanisms of solute diuresis
    • Glucosuria in diabetes; hyperglycemia leads to osmotic diuresis.
    • Iatrogenic solute diuresis: mannitol, radiocontrast, high-protein feeding increasing urea production.
    • Salt-wasting tubulopathies and tubulointerstitial diseases can also cause natriuresis and polyuria, especially during recovery from ATN or after obstruction relief.
  • Large-volume dilute urine (polyuria) etiologies
    • Polydipsia (habit, psychiatric, neurologic lesions, certain meds): extracellular fluid normal or expanded; low AVP; urine osmolality very low (~50 mosmol/L in primary polydipsia).
    • Diabetes insipidus (central vs nephrogenic): distinction via plasma AVP, copeptin, and responses to water deprivation and desmopressin (DDAVP).
  • Diagnostic plan for polyuria (Fig. 55-4 concept)
    • Assess volume status, measure urine osmolality to classify diuresis.
    • Consider central DI vs nephrogenic DI via AVP/copeptin levels and desmopressin testing when indicated.
    • A water deprivation test plus DDAVP can distinguish primary polydipsia, central DI, and nephrogenic DI; copeptin stimulation with hypertonic saline is an emerging alternative.
  • Additional notes on copeptin and AVP
    • Copeptin, a stable peptide cleaved from pre-pro-AVP, can be used as a surrogate marker for AVP in several centers.

Practical notes and clinical correlations

  • When assessing any patient with reduced kidney function, consider the full clinical context: volume status, hemodynamics, medication history (NSAIDs, ACEi/ARB), and prior imaging.
  • Urine sediment analysis is a powerful tool for distinguishing prerenal azotemia from intrinsic renal injury (ATN) and helps guide further testing and management.
  • Urinary casts and sediment findings often drive whether a kidney biopsy is pursued to establish a definitive diagnosis.
  • The nephrotic vs nephritic distinction has important therapeutic and prognostic implications; proteinuria amount and composition guide differential diagnoses and management strategies.
  • There is a strong link between GFR estimation and drug dosing; inaccurate GFR estimates can lead to drug toxicity or under-dosing.
  • Ethical and practical considerations in modern eGFR estimation include race modifiers and their implications for access to transplantation and treatment decisions; ongoing evaluation of alternative markers (e.g., cystatin C) is important.

Quick reference: key formulas and thresholds

  • GFR direct measurement (inulin/iothalamate clearance):
    • GFR=UimesVPGFR = \frac{U imes V}{P}
    • Where U = urine concentration of tracer, V = urine flow rate, P = plasma concentration of tracer.
  • Creatinine clearance (CrCl):
    • CrCl=U<em>extvolimesU</em>extCrP<em>extCrimesT</em>extminCrCl = \frac{U<em>{ ext{vol}} imes U</em>{ ext{Cr}}}{P<em>{ ext{Cr}} imes T</em>{ ext{min}}}
  • Urine Na and osmolarity patterns in prerenal azotemia vs ATN (Table 55-2)
    • Prerenal azotemia: UNa < 20 mmol/L; urine osmolality > 500 mosmol/L; FENa < 1%; UCr/PCr > 40.
    • Oliguric ATN: UNa > 40 mmol/L; urine osmolality < 350 mosmol/L; FENa > 2%; UCr/PCr < 20.
  • BUN/PCr ratio in prerenal azotemia: > 20:1.
  • Fractional excretion of sodium (FENa):
    • FENa = rac{(U{Na} imes P{Cr})}{(P{Na} imes U{Cr})} imes 100 o rac{ ext{%}}{}
  • Albumin-to-creatinine ratio (ACR):
    • ACRext(mg/g)≈AER (mg/24 h)ACR ext{ (mg/g)} \approx \text{AER (mg/24 h)}
  • Nephrotic-range proteinuria: >
    • > 3.5 ext{ g/day (per 1.73 m}^2)
  • CKD-EPI equation (typical form)
    • eGFR=141imesextmin(Scrκ,1)αimesextmax(Scrκ,1)−1.209imes0.993extAgeimes[1.018extiffemale]imes[1.159extifBlack]eGFR = 141 imes ext{min}\bigg(\frac{Scr}{\boldsymbol{\kappa}}, 1\bigg)^{\boldsymbol{\alpha}} imes ext{max}\bigg(\frac{Scr}{\boldsymbol{\kappa}}, 1\bigg)^{-1.209} imes 0.993^{ ext{Age}} imes [1.018 ext{ if female}] imes [1.159 ext{ if Black}]
    • with Scr = serum creatinine, κ = 0.7 (female) or 0.9 (male), α = −0.329 (female) or −0.411 (male).
  • Kidney anatomy and barrier concepts
    • Glomerular barrier prevents most large proteins; the glomerular basement membrane traps large proteins; podocyte slits (slit diaphragms) allow small solutes but not proteins.
    • Selective (albumin-only) vs nonselective proteinuria depends on the integrity of the filtration barrier.

Connections to earlier and later chapters

  • Foundations in renal physiology (GFR regulation, autoregulation, RAAS, prostaglandins) underpin prerenal azotemia and NSAID/ACEi interactions (Chapter discussions on renal hemodynamics).
  • Proteinuria evaluation ties into glomerular biology and nephrotic syndrome discussions (Chapter 326); tubular proteinuria vs glomerular proteinuria distinction links to nephron segment functions.
  • Urinary sediment interpretation relates to glomerulonephritis and tubulointerstitial diseases (Chapter 328); dysmorphic RBCs and RBC casts guide biopsy decisions (Fig. 55-2).
  • Diagnostic approaches to AKI (prerenal vs intrinsic vs postrenal) connect with broader AKI management strategies and therapies discussed in Brenner and Rector’s The Kidney and related chapters.

Ethical and practical implications

  • Race modifiers in eGFR calculations have social and clinical consequences; ongoing reassessment aims to avoid disparities in transplant listing and drug dosing.
  • The choice between creatinine-based and cystatin C–based eGFR involves balancing accuracy, accessibility, and patient-specific factors (muscle mass, inflammation, obesity, malnutrition).
  • Biopsy decisions weigh diagnostic yield against procedural risks; management depends on precise etiologies (glomerular vs interstitial vs vascular).
  • Early identification and treatment of AKI risk factors (nephrotoxins, dehydration, hypotension) can reduce progression to ATN and the need for dialysis.

Appendix: abbreviations used

  • BUN: blood urea nitrogen
  • PCr: plasma creatinine concentration
  • PNa: plasma sodium concentration
  • UCr: urine creatinine concentration
  • UNa: urine sodium concentration
  • FeNa: fractional excretion of sodium
  • GFR: glomerular filtration rate
  • CrCl: creatinine clearance
  • ACR: albumin-to-creatinine ratio
  • AKI: acute kidney injury
  • ATN: acute tubular necrosis
  • AIN: allergic interstitial nephritis
  • DI: diabetes insipidus
  • DDAVP: desmopressin (vasopressin analog)
  • copeptin: surrogate marker for AVP
  • CKD-EPI: Chronic Kidney Disease Epidemiology Collaboration equation
  • MDRD: Modification of Diet in Renal Disease equation
  • ANCAs: antineutrophil cytoplasmic antibodies
  • RBC: red blood cell
  • WBC: white blood cell
  • UTI: urinary tract infection
  • TB: tuberculosis
  • MAG3: mercaptoacetyltriglycine (nuclear medicine renal scan)
  • SBP: systolic blood pressure, DBP: diastolic blood pressure