Internal exam (nephrology)

N1. Urinalysis: correct collection, types and interpretation of findings

Collection

• Avoid contamination: hand hygiene, gloves, clean external genitalia

• Use sterile urine container

• Best sample: morning midstream urine, about 30 mL

• Avoid collection during menstruation or after strenuous exercise

• Close, label and send to lab quickly

• Analyze within 2 hours. If delayed: refrigerate / preserve

• Do not use urine from urine bag

• Ideally patient should not be on antibiotics

Types

• Gross assessment: volume, color, odor, turbidity, specific gravity

• Sediment microscopy: cells, casts, crystals, organisms, fat bodies

• Dipstick / chemical: pH, protein, glucose, ketones, blood, leukocyte esterase, nitrite, urobilinogen

• Other tests: osmolality, electrolytes, ACR, culture

Interpretation

• Color: dark = dehydration; red = hematuria; orange = liver/bile disease; blue-green = Pseudomonas/dye; purple = UTI

• Odor: ammonia = UTI; sweet = diabetes/ketoacidosis/MSUD; musty = liver disease/PKU

• Turbidity: cloudy = UTI; milky = chyluria/UTI; foamy = proteinuria; sediment = crystals/UTI

• pH: normal 4.8–7.6; acidic in starvation/drugs/kidney dysfunction; alkaline in UTI/vegan diet/kidney dysfunction

• Specific gravity: <1.005 = overhydration; >1.030 = dehydration

• Dipstick positives: protein, glucose, ketones, blood → proteinuria, glycosuria, ketonuria, hematuria

N2. Urine sediment microscopy: how to perform, what are the findings

Performing

• Correct urine collection: fresh midstream morning urine

• Centrifuge 5–10 min, 1500–2000 rpm

• Remove supernatant, resuspend sediment

• Place drop on slide + cover slip

• Examine by light/phase-contrast microscopy

• Use polarized light for crystals

Findings

• RBCs: hematuria, nephritic syndrome

• WBCs: pyuria/sterile pyuria, AIN

• Crystals: nephrolithiasis, e.g. Ca-oxalate, uric acid, struvite

• Organisms: bacteria/UTI

Casts

• Hyaline = normal possible

• RBC = nephritic syndrome

• WBC = pyelonephritis

• Fatty = nephrotic syndrome

• Epithelial/granular muddy brown = ATN

• Waxy = CKD

N3. Microalbuminuria: definition, detection, clinical significance

Definition

• Albumin excretion 30–300 mg/24 h

• Normal: <30 mg/24 h

Detection

• Spot UACR = most practical (albumin-creatinine ratio)

• Albumin dipstick

• 24 h urine collection

• Timed collection

• Diagnosis: 2/3 positive tests

Clinical significance

• Earliest sign of diabetic nephropathy, also hypertensive nephropathy

• Indicates early glomerular/endothelial injury before GFR falls

• Predicts CKD progression + cardiovascular risk

• Guides ACEI/ARB, BP and glycaemic control

• Can be reversible early

N4. Quantitative and qualitative methods to detect proteinuria

Quantitative

• Exact protein amount; used for diagnosis/monitoring/staging

• UACR: spot urine albumin mg/creatinine g

• UPCR: spot urine total protein mg/creatinine g

• 24 h urine protein: gold standard

Qualitative

• Screening/presence/type of protein

• Dipstick: mainly albumin, insensitive to non-albumin proteins

• SSA (Sulfosalicylic acid) test: detects all proteins by turbidity: albumin, globulins, light chains

• Electrophoresis (UPEP): detects abnormal protein bands, e.g. Bence-Jones proteins

N5. Acute kidney injury: definition, terminology, classifications

Definition

• AKI = rapid fall in GFR

• Causes ↑ creatinine, ↑ urea and retained metabolites

• Not one disease, but manifestation of different pathologies

Terminology

• AKI is preferred because reduced kidney function can occur without structural injury

• Examples: hypotension ↓GFR; drugs ↑creatinine by secretion competition

Clinical classification

• Pre-renal: renal hypoperfusion without intrinsic damage

• Intra-renal: parenchymal damage to tubules/glomeruli/interstitium

• Post-renal: urinary obstruction → ↑intratubular pressure → ↓GFR

Staging systems

• RIFLE: Risk, Injury, Failure, Loss, ESRD

• AKIN: simplified RIFLE + early creatinine rise

• KDIGO: current standard, stages 1–3 by creatinine + urine output

N6. AKI: distinguish pre-renal, renal and post-renal types

Pre-renal AKI

• Perfusion problem; kidney structurally intact

• Causes: hypovolemia, vomiting/diarrhoea, dehydration, haemorrhage, burns

• Also CHF, liver failure, nephrotic syndrome, renal artery stenosis, NSAIDs, ACEI/ARB

• Labs: BUN:Cr >20:1, FENa <1%, osm >500, SG >1.020

Intra-renal AKI

• Kidney parenchymal damage

• Causes: ATN/ATI, AIN, GN, TMA/DIC, hypertensive crisis

• Also rhabdo, hemolysis, TLS, myeloma, drugs/toxins

• Labs: BUN:Cr <15:1, FENa >2%, osm <350, SG <1.010

Post-renal AKI

• Urine outflow obstruction

• Causes: stones, tumor, BPH, neurogenic bladder

• Early = pre-renal pattern; late = intra-renal pattern

Annotation

• Pre-renal → labs

• Renal → sediment

• Post-renal → ultrasound

N7. Commonly used medications which may cause AKI, pathogenesis of decreased GFR

Pre-renal drugs

• NSAIDs, ACEI/ARB, diuretics, calcineurin inhibitors

Intra-renal drugs

• ATN: aminoglycosides, vancomycin, amphotericin B, contrast, cisplatin, tenofovir/adefovir, myoglobin/hemoglobin

• AIN: penicillins, cephalosporins, NSAIDs, PPIs, allopurinol, sulfa drugs

Post-renal drugs

• Anticholinergics/opioids → urinary retention

• Indinavir → stones

Pathogenesis

• Pre-renal: ↓perfusion pressure → ↓filtration pressure → ↓GFR

  • NSAIDs: afferent constriction

  • ACEI/ARB: efferent dilation

• Renal: tubular cell injury/death → casts + obstruction/backleak → ↑intratubular pressure → ↓GFR

• Post-renal: obstruction → back pressure opposes filtration → ↓GFR; chronic obstruction → tubular atrophy

N8. Oliguric phase of acute kidney injury (insufficiency): symptoms, lab findings, management

Oliguric phase

• 2nd AKI phase, lasts 1–2 weeks

• Kidney damage with urine output <400 mL/day

Symptoms

• Oliguria/anuria

• Oedema, hypertension, weight gain

• Uremia: fatigue, weakness, confusion, nausea/vomiting

• Electrolyte symptoms: cramps, weakness, arrhythmias

Labs

• ↓GFR, ↑BUN, ↑creatinine

• ↑K⁺

• Metabolic acidosis: ↓pH, ↓HCO₃⁻, ↑anion gap

• FENa/SG/osmolality/sediment depend on AKI type

Management

• Treat cause + stop nephrotoxins

• Monitor input/output + daily weight

• Fluid overload: furosemide if needed

• ECG monitoring

• Hyperkalemia if K⁺ >6 or ECG changes:

  • Calcium gluconate

  • Insulin + glucose IV

  • Furosemide / dialysis

• Acidosis: IV sodium bicarbonate if needed

• CRRT/acute dialysis if indicated

• Diet: low K⁺, phosphate, Na⁺ and protein

N9. Polyuric phase of acute kidney injury (insufficiency): symptoms, lab findings, management

Polyuric phase

• 3rd AKI phase, lasts up to 3 weeks

• Urine output rises, but tubules cannot concentrate/reabsorb well

Symptoms

• Polyuria >3–6 L/day

• Hypovolemia: dehydration, dry mucosa, hypotension, tachycardia, orthostasis

• Electrolyte loss: K⁺, Na⁺, Mg²⁺ loss → weakness, dizziness, arrhythmias

Labs

• ↑GFR

• ↓BUN, ↓creatinine

• ↓K⁺ and other electrolytes

• Metabolic acidosis may persist from HCO₃⁻ loss

Management

• Monitor input/output

• Careful fluid replacement, usually isotonic fluids

• Correct electrolytes, especially IV K⁺ if needed

• Avoid dehydration and fluid overload

• Correct symptomatic acidosis

• Supplement protein, vitamins, electrolytes

N10. Indications for immediate start of dialysis (HD/PD)

Definition: Procedure to remove waste/fluid and corrects acidosis, electrolyte imbalance and removes toxins

AEIOU indications

• A — Acidosis: pH <7.1, refractory

• E — Electrolytes: hyperkalaemia >6.5 mmol/L, ECG changes or refractory

• I — Intoxication: lithium, methanol, isopropanol, salicylates, ethanol

• O — Overload: pulmonary oedema/fluid overload resistant to diuretics

• U — Uremia: encephalopathy, pericarditis, neuropathy, bleeding, nausea/vomiting, inability to eat

  • Urea >35 mmol/L, BUN >100, eGFR <15 when clinically indicated

Types

• Hemodialysis: preferred emergency/acute setting; rapid effect

  • Acute access: central venous catheter

  • Long-term: AV fistula/graft

• Peritoneal dialysis: slower, stable/long-term outpatient, young active pts.

  • Peritoneum = semipermeable membrane

  • Access: peritoneal catheter

  • Modalities: CAPD, APD

N11. Detection methods and markers of glomerular filtration rate

Direct/measured GFR

• More exact but complicated

• Inulin clearance: gold standard; freely filtered, not reabsorbed/secreted

• Iohexol clearance

• Radioisotope clearance/scintigraphy: Cr-EDTA, Tc-DTPA

Estimated GFR

• Used clinically

• Creatinine clearance: 24 h urine + serum creatinine + urine volume; Cockcroft-Gault

• **Serum creatinine: CKD-EPI, MDRD

• Serum cystatin C: cystatin C equations, can combine with creatinine

• Schwartz formula: pediatric population

Markers of GFR

• Inulin clearance, iohexol clearance, radioisotope clearance

• Creatinine clearance, cystatin C clearance

Markers of eGFR

• serum creatine, serum cystatin C

• eGFR formulas: CKD-EPI, MDRD, Schwartz, Cockcroft-Gault