Renal



Renal


Shana McCormack

Paritosh Prasad

Avram Z. Traum



Urinalysis


Evaluation

(Pediatr Clin North Am 2006;53:325)






















































Urine Dipstick Test Finding Nonpathologic Causes Pathologic Causes
Specific gravity (low) Polydipsia DI, renal tubular dysfunction
Specific gravity (high) Inadequate volume intake Volume depletion
pH (low) High-protein diet Acidosis
pH (high) Low-protein diet; recent meal RTA (inappropriate renal response); UTI (ie. Proteus)
Blood present (can represent RBCs, Hgb, myoglobin) Menses, traumatic catheterization, exercise Glomerular d/o, tubular d/o, UTI, stones, hypercalciuria, urinary tract trauma, tumor rhabdo, hemolysis
Protein present Orthostatic proteinuria, fever, exercise Glomerular disorders, tubular disorders, UTI
Glucose present Renal glycosuria (SGLT2 transporter defect) Diabetes mellitus, Fanconi anemia
Ketones Restricted carbohydrate intake Diabetes mellitus starvation, EtOH
Bilirubin present None Hepatitis, biliary obstruction
Urobilinogen present Low amounts: systemic Abx Rx Hepatitis, intravascular hemolysis
Nitrite present None UTI (Enterobacteriaceae only), bacturia
LE present (from PMNs) Fever UTI, glomerulonephritis, pelvic inflamm, sterile pyuria



  • Urine protein/Cr ratio correlates w/ total daily protein excretion based on g/1.73 m2 BSA. Low Cr in cachectic child or ↓ muscle mass (e.g., myopathy, myelomeningocele) may overestimate ratio. Nml ratio <0.2 mg protein/mg Cr.


  • Urine albumin/Cr ratio correlates w/ excretion of albumin in timed sample. Ratio >30 mg/g Cr abn. (Nml albumin excretion <20 mg/d), and microalbuminuria defined as 30–300 mg/d, and not typically detected on U/A.


  • Urine calcium/Cr ratio correlated w/ excretion of Ca++ in a timed sample. Nml ratio depends on age; in school-aged children and adolescents, should be <0.21.


Acute Renal Failure


Definition

(Adolesc Med Clin 2005;16:1)



  • Sudden onset, inadeq renal fxn to clear metab waste, maintain nml fluid and electrolyte balance. May be oliguric (30%) or urine output may be nml to ↑ (70%).


Epidemiology

(Pediatr Rev 2002;23:47; Am J Kidney Dis 2005;45:96)



  • Epidemiology of renal failure changed in face of advances in pediatric ICU care, congenital heart surgery, and pediatric oncology/bone marrow transplantation.



    • Previously intrinsic renal disease was felt to be the most common cause of ARF


    • Now ARF is most commonly found as a morbidity assoc w/ other systemic illness


  • Retrospective review at 3° care pedi hospital w/ most common causes ARF to be renal ischemia (21%), nephrotoxic medications (16%), and sepsis (11%).


  • In developing countries, 3 most common causes of ARF are: Hemolytic-uremic syndrome (31%), glomerulonephritis (23%), prerenal ischemia (18%)





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Etiology

(Adolesc Med Clin 2005;16:1)



  • Pre-renal: renal hypoperfusion (intravasc volume loss 2/2 dehydration, trauma, capillary leak from sepsis/burns/nephrotic syndrome, poor cardiac function)


  • Post-renal: structural/obstructive causes (rare, 2/2 pelvic mass or ureteral obstruct)


  • Intrinsic-renal: underlying kidney injury or dz



    • Endogenous toxins: Hgb, myoglobin, or uric acid in tumor lysis


    • Exogenous toxins: NSAIDs, Abx, antifungals, chemo, contrast, ACE-I in some


    • Allergic rxn/interstitial nephritis


    • Infxn: Pyelo, postinfectious syndromes, such as post-Streptococcal GN or HUS


    • Immune-mediated vasculitides: SLE, polyarteritis, Wegener, Goodpasture


    • Vascular; renal artery or vein thrombosis of a single or transplanted kidney


Diagnostic Evaluation

(Pediatr Rev 1995;16:101; Pediatr Rev 2002;23:47)



  • Complete H&P focused on narrowing the above differential


  • Initial labs: U/A w/ microscopy & culture, CMP, CBC, sediment


  • Fractional excretion (FE) Na = (PCr × UUN)/(BUN × UCr) (inaccurate w/ diuretics)



    • PCr is plasma conc of Cr; PNa is plasma conc of Na


    • UCr is urinary conc of Cr, and UNa is urinary conc of Na.


    • FENa <1%; ↓ renal perfusion, w/ hypovolemia, low cardiac output states.


    • FeNa >2%; spilling Na, makes intrinsic renal dz more likely (i.e., ATN).


  • FE Urea = (PCr × UUN)/(BUN × UCr); <35%–40% prerenal (use if on diuretics)


  • Glomerular filtration rate (mL/min/1.73 m2) calculated as length (cm) × (K/plasma Cr conc), (K is coefficient 0.45 for <1–12 mo; 0.55 for 2–12 yo and older girls, and 0.7 for boys 13–18 yo via the Schwartz formula.



    • Creatinine clearance (CrCl) is a surrogate marker of GFR.


  • Consider: Albumin, cholesterol, serum complement, antinuclear Ab, streptococcal serologies, blood and stool cultures, toxicology screen


  • Imaging may include ultrasound, CT, MRI/MRA; biopsy may be indicated


Therapy

(Adolesc Med Clin 2005;16:1)



  • Etiology dependent; please see sections on specific dx under proteinuria/hematuria


  • Monitor BP, volume status, serum chemistries (specifically, ARF produces hyperkalemia, as the kidneys are responsible for 90% of renal potassium excretion) and acid-base status (specifically, ARF produces metabolic acidosis)


  • Avoid nephrotoxic agents and dose all meds according to estimated CrCl


  • Renal replacement Rx (dialysis, CVVH) indicated for life-threatening volume overload, hyperK, hypoNa, metabolic acidosis refractory to medical mgmt, complications of uremia (pericarditis, encephalopathy), or to clear toxins


Prognosis

(Arch Pediatr Adolesc Med 2002;156:893)



  • Dependent on underlying etiology, much worse if multiorgan involvement; >50% mortality if three or more organs are involved


Chronic Renal Failure


Definition

(Pediatr Nephrol 2003;18:796)



  • Chronic renal insufficiency is defined as CrCl <75 mL/min/1.73 m2.


Etiology

(Pediatr Nephrol 2003;18:796)



  • ∼40% w/ congenital urologic anomalies.


  • Causes of CRI (↓ order prevalence): Obstructive uropathy, aplastic/hypoplastic/dysplastic kidneys, reflux nephropathy, FSGS, polycystic kidney dz, immunologic dz, syndrome of agenesis of abd musculature, renal infarction, HUS, cystinosis, others, unknown.


Complications

(Pediatr Nephrol 2003;18:796)



  • Infections prompt 45% of hospital admissions in one series.


  • Other potential complications include: Anemia, hypertension bone disease.


  • Short stature is common (one series shows delay of -1.4 SD at the time of registry to a CRI database); recombinant growth hormone is one possible therapy.


Prognosis

(Pediatr Nephrol 2003;18:796; J Am Soc Nephrol 2005;16:2796)



  • Proteinuria, low Hct, hypoalbuminemia, hypoCa, hyperphos, hyperPTH all assoc w/ rate of progress to ESRD, as is age at dx and the dx itself.


  • Rx of anemia, hypoCa, and hyperphos leads to improved outcomes in the short-term



  • Cardiac and vascular abn (LVH, diastolic dysfxn, ↑ carotid intima-media thickness) are progressive and may be related to ↑ calcium-phosphorus product.


  • Glomerular disorders, including FSGS, increase risk of progression to ESRD.


Secondary Hypertension


Definition

(Pediatr Rev 2007;28:283)



  • 2° HTN (BP >95th percentile for age and ht) – ↑ BP 2/2 underlying, identifiable cause

Jun 19, 2016 | Posted by in PEDIATRICS | Comments Off on Renal

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