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Renal disorders
Llewellyn F Mensah, MD
OVERVIEW
Functions of the kidneys
Assessment of renal function
Acute kidney injury
Chronic Kidney Disease
Board review
Functions of the
kidneys
Maintenance of constant extracellular environment
(excretion of waste products of metabolism such as
urea, creatinine, uric acid and water/electrolyte
balance)
Secretion of hormones that participate in the
regulation of systemic and renal hemodynamics
 renin, angiotensin and bradykinin
 EPO (RBC production)
 1,25 – dihydroxyvitamin D3 or calcitriol (Calcium,
phosphorus and bone metabolism)
ASSESSMENT OF RENAL
FUNCTION
GFR and its assessment
Urinalysis
Radiologic evaluation
Serology
Proteinuria
GFR
A rough measure of the number of functioning nephrons
~ 130 mL/min/1.73 m2 for men and 120 mL/min/m2 for women
with considerable variation
GFR decreases somewhat with age
GFR = Cx = (Ux x V)/ Px
Gold standard for x is inulin (freely filtered, neither secreted,
reabsorbed, synthesized nor metabolized)
In the United States, GFR most commonly measured using
creatinine clearance or equations based on serum creatinine,
age, weight (Cockcroft-Gault, MDRD, CKD-EPI)
Cystatin C is most commonly used in research settings (more
sensitive for detection of mild reductions in renal function
therefore suggested for use in the elderly, children, renal
transplant recipients, patients with cirrhosis)
Diagnostic approach urinalysis
Urinary pattern
Kidney disease suggested by pattern
Hematuria with dysmorphic RBCs, RBC
casts, varying degrees of albuminuria
Proliferative GN (eg IgA nephropathy, ANCA associated
vasculitis, lupus nephritis)
Heavy albuminuria with minimal or
absent hematuria
Non proliferative glomerulopathy (eg diabetes,
amyloidosis, membranous nephropathy, FSGS, minimal
change)
Multiple granular and epithelial cell
casts with free epithelial cells
Acute tubular necrosis in a patient with underlying AKI
Isolated pyuria
Infection or tubulointerstitial disease
Dipstick positive for blood but no RBCs
on microscopy
Rhabdomyolysis (clear serum), Hemolysis (pigmented
serum)
Eosinophils and possibly WBC casts
Allergic interstitial nephritis
Normal UA with few cells, no casts, and
no or minimal proteinuria
AKI: pre renal disease, UTO, myeloma cast nephropathy
CKD: Ischemic nephropathy, hypertensive
nephrosclerosis, UTO, hepatorenal disease, cardiorenal
disease
Uric acid
Calcium oxalate
cystine
Magnesium ammonium
phosphate
Bacteria, budding
yeasts, hyphae
Red blood cells
White blood cells
Renal tubular cells
Transitional epithelial
cells
Squamous epithelial
cells
RBC casts
WBC casts
Renal tubular epithelial
cell casts
Granular casts
Hyaline casts
Fatty casts
Radiologic evaluation
Renal U/S – cortical thinning and decreased kidney
size, UTO, complications of pyelonephritis
Doppler renal ultrasonography – evaluation of renal
vascular flow (renal vein thrombosis, renal
infarction, renal artery stenosis)
Non contrast enhanced helical CT scanning - gold
standard for nephrolithiasis
MRI – renovascular hypertension, renal vein
thrombosis, renal masses
Renal arteriography - PAN (aneurysms/renal artery
constrictions)
Radionuclide scans
 Tc99mMAG3 - differentiation between obstructive and
non obstructive hydronephrosis and identification of
differences in function of the kidneys in infants and
children (less radiation exposure compared to CT
scanning)
 DMSA / Tc99m succimer - used for better assessment
of focal renal parenchymal abnormalities / renal
function
Serology
Useful for glomerular disease (nephritic / nephrotic)
Done before renal biopsy to aid in diagnosis
Nephrotic (proteinuria > 3.5 g/d, hypoalbuminemia,
hyperlipidemia, edema)
 Lupus (ANA, anti – dsDNA, c3, c4), HBV, HCV, HIV
Nephritic (red cells/red cell casts, hypertension)
 post infectious (C3, C4, antiDNAse B, ASOT),
Wegener’s (anti GBM antibodies, ANCA), HBV, HCV
Proteinuria
Most accurately measured by the 24 hour urine
protein excretion
More convenient to measure spot first or second
early morning urine protein to creatinine ratio as an
estimate of this value but not very accurate
The normal daily protein excretion is less than 150 mg
(> 300 mg if pregnant)
A patient with isolated proteinuria (normal UA and
renal function) should be evaluated for transient
proteinuria and orthostatic proteinuria
If these are ruled out, referral to a nephrologist is
indicated
UPCR to estimate
protein excretion
Acute kidney injury
Definition
 AKI: abrupt (< 48 h) increased creatinine ≥ 50%, or UOP
< 0.5 mL/kg/h for ≥ 6 h. Cannot estimate GFR using
creatinine in setting of AKI or changing creatinine
(requires steady state)
Workup
 H&P: recent procedures and meds; thirst; VS and
volume; s/s of obstruction, vascular or systemic
disease; ischemia (pre renal/ATN) accounts for > 50% of
in – hospital AKI
Accepted diagnostic criteria include




increase in creatinine of 0.5 mg/dL
50% increase in the creatinine level above baseline
50% decrease in the baseline calculated GFR, or
need for acute kidney replacement therapy
Prevalence in US
 1% (community acquired)
 up to 7.1 % (hospital acquired) of all hospital
admissions
 Non ICU mortality rate is ~ 10%
Affects 15 – 20 % of patients in ICUs
 Reported mortality rates > 50%; up to 80% if renal
replacement therapy or dialysis required
Most common causes of death are
 infection complications
 Cardiorespiratory complications
Pathophysiology
Creatinine is a metabolic waste product excreted by
the kidneys
Normal GFR
 filtered through the glomerulus into the tubules then
excreted
 also secreted by tubular cells
Certain medications can inhibit tubular secretion and
falsely elevate the serum creatinine level (bactrim,
cimetidine)
Risk factors for ARF
Concurrent
Concurrent disease
nephrotoxic drugs states
Patient findings
Furosemide
Advanced age
Neoplasia,
hypercalcemia
Chemotherapeutic Hemolytic anemia,
agents
hemoglobinuria
Dehydration
NSAIDs
Liver failure
Pre existing renal insufficiency
Pancreatitis
Shock, decreased CO
Heart failure
Thiamine
Fever
Electrolyte abnormalities
(hyponatremia, hypocalcemia,
hypokalemia)
Sepsis
Metabolic acidosis
Workup
 Urine evaluation: output, urinalysis, sediment,
electrolytes and osmolality
 Fractional excretion of sodium (FENa) =
(UNa/PNa)/(Ucr/PCr) < 1% - pre renal, contrast, HRS or
GN; > 2% leading to ATN.
 In setting of diuretics, check FEUN = (UUN/PUN) /
(Ucr/PCr); < 35% is diagnostic of pre renal AKI
 Renal U/S or CT: r/o obstruction and evaluate kidney
size to estimate chronicity of kidney disease
 Serologies
 Renal biopsy: may be necessary if cause remains
unclear (esp if hematuria and/or proteinuria)
Pre renal
 Intravascular volume depletion
 Diseases that lead to decreases in the effective arterial
blood volume
 NSAIDs, ACEI
 Large vessel disease
Intra renal





tubular
Glomerular
AIN
Vascular
CIAKI
Post renal
Pre renal azotemia
Intravascular volume depletion
 fever, vomiting and diarrhea can lead to decreased
kidney perfusion
 dehydration from any cause (diuretics) can precipitate
ARF
Diseases that lead to decreases in the effective
arterial blood volume
 heart failure
 liver failure
 nephrotic syndrome
Pre renal azotemia
NSAIDs
 Block cyclo oxygenase leading to increase in TXA2
then afferent vasoconstriction and decreased
glomerular perfusion
ACE inhibitors
 Block production of angiotensin II leading to
vasodilation postglomerular efferent vessels then
decreased glomerular pressure and possible azotemia
Large vessel disease
 Thrombosis, embolus, and dissection can lead to
reduced renal perfusion
Intra renal - Tubular
Injury most often caused by
 Ischemia and / or
 nephrotoxins
Acute tubular necrosis
 initiation
 maintenance
 recovery (marked diuresis and slow return of renal
function)
Intra renal - glomerular
Uncommon cause
Systemic manifestations
 fever
 rash
 arthritis
Urine findings
 RBC casts
 hematuria
 proteinuria
Renal consult and biopsy may be required
Intra renal - AIN
Allergic reaction to a drug (sulfonamides, allopurinol,
cephalosporins, ciprofloxacin, PCN, rifampin, thiazides,
furosemide, cimetidine, NSAIDs, phenytoin)
Autoimmune diseases
Infection
Infiltrative diseases
Symptoms - fever, rash, elevated serum and urine
eosinophils
Immediate withdrawal of drug and supportive care are
essential
Corticosteroids may be beneficial
Intra renal - vascular
Microvascular
 presents as microangiopathic hemolytic anemia and
ARF
 secondary to small vessel thrombosis or occlusion
Macrovascular
 renal artery stenosis or thrombosis
 atheroembolism secondary to AF, aortic disease, acute
dissection
Contrast induced AKI
Risk factors: CKD, DM, CHF, age, hypotension, increased
contrast volume
Clinical: Creatinine increase by 25% or 0.25 mg/dL within 48 h,
peaks in 3 – 5 days, resolves in 7 – 10 days
Prevention






Isotonic IV fluids (unless contraindicated eg CHF): 3 mL/kg/h x 1
hour, 1 mL/kg/h x 6 hour after NaHCO3 ? more effective than
NaCl
Hold ACEI/ARB, NSAIDs, diuretics
N-acetylcysteine 1200 mg PO bid on day prior to, and day of
contrast; safe and therefore reasonable in high risk patients,
but benefit remains unclear.
Minimize contrast volume and consider iso – osmolar contrast
? High dose statin
No proven benefit to prophylactic RRT in addition to above
(may actually be harmful)
Gadolinium:
 can cause AKI in stage IV CKD, no effective prophylaxis
 nephrogenic systemic fibrosis – fibrosis of skin, joints,
eyes and internal organs ~ 2 – 4 weeks post exposure
in patients with moderate – severe CKD ? role of
postgadolinium hemodialysis. Treatment is to improve
renal function, physical therapy. Can be irreversible
Post renal
Obstruction of the outflow tracts of the kidneys



prostatic hypertrophy
catheters
tumors
Most are readily reversible
Recovery of renal function is directly proportional to the
duration of the obstruction
Renal U/S recommended to assess for hydronephrosis
Systemic
manifestations of ARF
Fluids, electrolytes and
serum biochemical
disturbances
Gastrointestinal
disturbances
Hematological
disturbances
Anuria, oliguria,
polyuria/polydipsia
Anorexia
Platelet function
defect / bleeding
tendencies
Dehydration
Vomiting and diarrhea
Blood loss anemia
Azotemia
Halitosis
Lymphopenia
Metabolic acidosis,
Oral ulceration /
hyperphosphatemia,
stomatitis
hyperkalemia,
hypercalcemia/hypocalcemia
Peripheral insulin resistance
and glucose intolerance
Gastropathy, gastritis,
gastric and duodenal
ulceration and bleeding
neutrophilia
Systemic
manifestations of ARF
Cardiovascular and pulmonary
disturbances
Neuromuscular disturbances
Systemic arterial hypertension
Weakness
Uremic pneumonitis
lethargy
depression
Uremic encephalopathy
Coma / death
Etiologies
Prerenal
Intrinsic
Post
U/A Sediments, Indices
Decreased effective arterial volume: Hypovolemia,
decreased cardiac contractility (e.g. CHF), systemic
vasodilation (e.g. sepsis)
Renal vasoconstriction: NSAIDs, ACEI/ARB, contrast,
calcineurin inhibitors, HRS, hypercalcemia
Large vessel: RAS (bilateral + ACEI), VTE, vasculitis,
dissection, abdominal compartment syndrome
Bland
Transport hyaline casts
FENa < 1%
BUN/Cr > 20
UNa < 20
Uosm > 500
Acute tubular necrosis (ATN): ischemia (progression of pre
renal disease), toxins (drugs, pigments, proteins, crystals)
contrast induced AKI (decreased renal blood flow + toxin)
Pigmented granular muddy brown
casts in ~ 75% (+/- in CIAKI)
+/- RBCs and protein from tubular
damage
FENa > 2%, BUN/Cr < 20, UNa > 20
(except pigment, CIAKI)
Uosm < 350
Acute interstitial nephritis (Allergic, Infection, Infiltrative,
Autoimmune)
WBCs, WBC casts, +/- RBCs with
negative urine cx, urine eosinophils in
abx, urine lymphocytes in NSAIDs
Small medium vessel: cholesterol emboli, PAN, thrombotic
microangiopathy (HUS/TTP, DIC, pre eclampsia, APS,
malignant HTN, scleroderma renal crisis)
+/- RBCs, urine eosinophils
Bladder neck: (BPH, prostate cancer, neurogenic bladder,
anticholinergic meds)
Ureteral (bilateral): malignancy, lymphadenopathy,
retroperitoneal fibrosis, nephrolithiasis
Bland +/- nondysmorphic RBCs, FENa
variable
Alternative
classification
Nephrosis

renal ischemia (dehydration, hypovolemic shock, sepsis,
burns, heat stroke, DIC, decrased CO, thromboembolism,
vasculitis, HTN, hyperviscosity, multiple myeloma,
polycythemia, hemoglobin/myoglobin, NSAIDs, acute
decompensation of CRF
 nephrotoxicosis (ethylene glycol, antibiotics,
chemotherapeutics, anesthetics, heavy metals,
hypercalcemia, CCl4, chloroform, contrast)
Nephritis

infections (leptospirosis, leishmaniasis, bacterial
pyelonephritis)
 inflammatory (glomerulonephritis, allergic / drug induced)
Treatment
Therapy is directed at treating the underlying cause
Correcting
 fluid imbalance
 electrolyte abnormalities
 uremia
Preventing complications
 including nutritional deficiencies
Treatment
Treat underlying disorder ? Steroids if acute
interstitial nephritis
Prerenal: Isotonic IVF is pretty much same as
albumin; HES is nephrotoxic
Avoid nephrotoxic insults; review dosing of renally
cleared drugs
Optimize hemodynamics (both MAP and CO); may
take 1 – 2 weeks to recover from ATN
Watch for, and correct volume overload, electrolytes
(hyperkalemia, hyperphosphatemia), and acid base
status
Hyperkalemia
Calcium

calcium gluconate 10% solution – 10 mL IV
Insulin

10 units IV and glucose 25 g
Inhaled beta agonists
Sodium bicarbonate

3 ampoules in 1 L of 5% dextrose
Sodium polystyrene sulfonate (kayexalate)


orally 25 – 50 g mixed with 100 mL of 20% sorbitol
rectally 50 g in 50 mL of 70% sorbitol and 150 ml of tap water
Dialysis (last resort)
Acidosis
Sodium bicarbonate (if serum level < 15 mEq/L or pH <
7.2)
 given IV or PO
 amount based on bicarb deficit equation (0.4 x wt x
{24 – serum bicarb})
 arm and hammer baking soda provides approximately
50 mEq of NaHCO3 per rounded tsp
Dialysis
 required for irretractable acidosis
 20 – 60% of patients when BUN is > 100 or Cr is 5 - 10
If obstruction is diagnosed and relieved, watch for
 hypotonic diuresis (2/2 buildup of BUN, tubular
damage); treat with IVF eg ½ NS
 hemorrhagic cystitis (rapid change in size of bladder
vessels); avoid by decompressing slowly
Indications for urgent dialysis (when condition is
refractory to conventional therapy)
 Acid base disturbance: acidemia
 Electrolyte disorder: generally hyperkalemia;
occasionally hypercalcemia, tumor lysis
 Intoxication: methanol, ethylene glycol, lithium,
salicylates
 Overload of volume (CHF)
 Uremia: pericarditis, encephalopathy, bleeding
No benefit to dopamine or mannitol
CKD
≥ 3 months of reduced GFR (< 60) and/or kidney damage
(path, markers, imaging)
Prevalence 13% in US; Cr poor estimate of GFR in patients,
therefore use prediction equation eg MDRD or CKD – EPI
(may underestimate GFR in patients with normal renal
function esp MDRD)
Etiologies: DM (45 %), HTN/RAS (27 %), glomerular (10 %),
interstitial (5 %), PKD (2%), congenital, drugs, myeloma,
progression of AKI
Presence and degree of albuminuria associated with
worse outcomes independent of GFR
Rates of all cause mortality and CV events increase with
each stage of CKD and are significantly higher than the
rate of progression to kidney failure
Stages of CKD
Stage
GFR
Goals
1 (normal or
increased GFR)
> 90
Dx/Rx of underlying condition and
comorbidities, slow progression;
cardiovascular risk reduction
2 (mild)
60 - 89
Estimate progression
3 (moderate)
30 – 59
Evaluate and treat complications
4 (severe)
15 – 29
Prepare for RRT
5 (renal failure)
< 15 or
dialysis
Dialysis if uremic
Signs and symptoms of uremia
General
Nausea, anorexia, malaise, fetor uremicus, metallic taste,
susceptibility to drug overdose, decreased temperature
Skin
Uremic frost, pruritus, calciphylaxis, NSF
Neurologic
Encephalopathy, seizures, neuropathy, impaired sleep,
restless legs syndrome
Cardiovascular Pericarditis, accelerated atherosclerosis, hypertension,
hyperlipidemia, volume overload, CHF, cardiomyopathy
(esp LVH)
Hematologic
Anemia, bleeding
Metabolic
Hyperkalemia, hyperphosphatemia, acidosis, hypocalcemia,
secondary hyperparathyroidism, osteodystrophy
Causes of CRF that lead
to ESRD and transplant
Chronic glomerulonephritis
Diabetic nephropathy
Hypertensive nephropathy (~ 25% of cases)
Polycystic kidney disease
Chronic pyelonephritis
Renal calculi
Treatment
General: nephrology referral when GFR < 30 and
access planning (avoid subclavian lines; preserve an
arm for access by avoiding blood draws, BP
measurements, IVs); treat cardiovascular risk factors
(eg smoking, LDL), vaccines (flu, pneumonia, HBV)
Dietary restrictions: Na (if HTN), K (if oliguric or
hyperkalemic), PO4, ? moderate protein restriction,
strict glucose control in DM
BP control: goal < 140/90, start with ACEI (or ARB),
effective in DM and non diabetic CKD, likely no
benefit of ACEI + ARB. For outpatients, check
creatinine and K in 1 – 2 weeks, d/c if creatinine
increases 30% or K > 5.4 (after dietary change and
loop diuretic).
Metabolic acidosis: sodium bicarbonate or sodium
citrate if low HCO3
Anemia: goal Hb ~ 10 g/dL (worse outcomes if
higher). Epoetin (start 80 – 120 U/kg SC, divided 3x /
wk) or darbepoetin (0.45 ug/kg q wk); iron
supplementation to keep transferrin sat > 20% (often
given IV in HD patients)
Uremic bleeding: desmopressin (dDAVP) 0.3 ug/kg IV
intranasally
Lab evaluation
UA with microscopic exam
CMP and uric acid
Calcium and phosphorus
CBC
ANA, ANCA, SPEP
24 hr urine creatinine and protein
HBsAg, HCV antibody, HIV
C3, c4 and CH50
Anti – GBM antibody
Radiological evaluation
Renal U/S
Mag 3 renal scan
Renal angiogram
Voiding cystourethrogram
CT scan of the kidneys and liver
MRI
Renal biopsy
Hematuria with a low GFR or proteinuria
Nephrotic range proteinuria
CKD of unknown cause and normal or large kidneys
on U/S
ARF of unknown cause
Patient’s request
Renal biopsy
contraindications
Uncorrectable bleeding tendency
Small kidneys < 9 cm
Single (functioning) kidney
Severe HTN
Multiple large cysts
Hydronephrosis
Active infection
Monitoring CKD
eGFR should be obtained at least yearly in CKD, and
more often in patients with:





GFR < 60 mL/min/1.73 m2
fast GFR decline in the past
Risk factors for faster progression
Ongoing treatment to slow progression
Exposure to risk factors for acute GFR decline
Management of patients with
CRF before a dye study
Stop all diuretics and ACEI/ARB
D5W with 3 amps NaHCO3 1 cc/kg/hr at least 4 – 6
hours prior to exam
¼ NS with 2 amps NaHCO3 (patients with diabetes)
Mucomyst 1200 mg bid the day before and the day of
the exam
Secondary hyperparathyroidism:
Hyperphosphatemia, hypocalcemia, decreased
calcitriol leading to increased parathormone leading
to renal osteodystrophy
CKD Stage
3
4
5
Target PTH
35 – 70
70 – 110
150 - 300
Phosphorus binders (take with meals)
 if high PO4 and low Ca, use calcium acetate (phoslo) or
calcium carbonate
 if refractory high PO4 or in setting of high Ca, use
sevelamer (renagel), lanthanum (fosrenal)
 if severe hyperphosphatemia, use aluminium hydroxide
(amphojel), short term use only
Vitamin D or analogue (paricalcitol) if 25-OH vit D < 30
(stop if hypercalcemia)
Calcitriol or paricalcitriol if Ca-PO4 product < 55 (?
increased survival in HD patients)
Cinacalcet (parathyroid calcium sensing receptor
agonist) - if PTH remains elevated despite phosphate
binders +/- vit. D analogue
Parathyroidectomy
1. A 52-year-old female with a history of hypertension
and hypercholesterolemia presents with mild edema,
weakness, and body aches. Her only medications are
atorvastatin (Lipitor) and chlorthalidone. Her
previously normal serum creatinine level is now 2.6
mg/dL (N 0.64–1.27). Her BUN level is 32 mg/dL (N 6–
20) and her serum is clear without pigmentation. The
urine dipstick is positive for blood, but a microscopic
examination is negative for WBCs, RBCs, and Casts.
The most likely diagnosis is
A) allergic interstitial nephritis
B) glomerulonephritis
C) hemolysis
D) pyelonephritis
E) rhabdomyolysis
ANSWER: E
This patient with acute kidney injury (AKI) has clinical
symptoms and signs consistent with rhabdomyolysis, a
known cause of AKI. Furthermore, she is taking a
medication known to cause rhabdomyolysis. The urinalysis
with a positive dipstick for blood and no RBCs on the
microscopic examination is indicative of either hemolysis or
rhabdomyolysis. Darkened, pigmented serum would be
expected with hemolysis, while rhabdomyolysis is
associated with clear serum. Urine abnormalities found in
glomerulonephritis include proteinuria and RBC casts, while
patients with allergic interstitial nephritis may have
eosinophils and possibly WBC casts. Pyelonephritis is
associated with WBCs in the urine, and if the dipstick is
positive for blood there will be RBCs on the microscopic
examination.
A 52-year-old Hispanic female with diabetes mellitus
and stage 3 chronic kidney disease sees you for
follow-up after tests show an estimated glomerular
filtration rate of 56 mL/min. Which one of the
following medications should she avoid to prevent
further deterioration in renal function?
A) Lisinopril (Prinivil, Zestril)
B) Folic acid
C) Low-dose aspirin
D) Candesartan (Atacand)
E) Ibuprofen
ANSWER: E
Patients with chronic kidney disease (CKD) and those
at risk for CKD because of conditions such as
hypertension and diabetes have an increased risk of
deterioration in renal function from NSAID use.
NSAIDs induce renal injury by acutely reducing renal
blood flow and, in some patients, by causing
interstitial nephritis
Which one of the following is most commonly
implicated in interstitial nephritis?
A) NSAIDs
B) ACE inhibitors
C) Diuretics
D) Corticosteroids
E) Antibiotics
ANSWER: E
Antibiotics, especially penicillins, cephalosporins, and
sulfonamides, are the most common drug-related
cause of acute interstitial nephritis. Corticosteroids
may be useful for treating this condition. The other
drugs listed may cause renal injury, but not acute
interstitial nephritis.
A 4-year-old is brought to the emergency department
with abdominal pain and is noted to have 3+
proteinuria on a dipstick. Three days later the pain has
resolved spontaneously, and a repeat urinalysis in
your office shows 2+ proteinuria with normal findings
on microscopic examination. A metabolic panel,
including creatinine and total protein, is also normal.
Which one of the following would be most
appropriate at this point?
A) Renal ultrasonography
B) A spot first morning urine protein/creatinine ratio
C) An antinuclear antibody and complement panel
D) Referral to a nephrologist
ANSWER: B
When proteinuria is noted on a dipstick and the
history, examination, full urinalysis, and serum studies
suggest no obvious underlying problem or renal
insufficiency, a urine protein/creatinine ratio is
recommended. This test correlates well with 24-hour
urine protein, which is particularly difficult to collect in
a younger patient. Renal ultrasonography is
appropriate once renal insufficiency or nephritis is
established. If pathogenic proteinuria is confirmed, an
antinuclear antibody and/or complement panel may
be indicated. A nephrology referral is not necessary
until the presence of kidney disease or proteinuria
from a cause other than benign postural proteinuria is
confirmed.