Acute Kidney Injury (ATN)MANAGEMENT

GENITOURINARY AND REPRODUCTIVE PRESENTATIONS · 12 SECTIONS

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559 items

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Cardiovascular Presentations71▾

Respiratory Presentations52▾

Neurological Presentations83▾

Gastrointestinal Presentations74▾

Genitourinary and Reproductive Presentations48▾

Acute Kidney Injury (ATN)Acute Kidney Injury (Post-renal)Acute Kidney Injury (Pre-renal)Amniotic Fluid Embolism Balanitis Bladder Rupture Breast Abscess Cystitis Dialysis access complications Ectopic pregnancy Epididymitis Glomerulonephritis Hematuria (gross)Hydrocele Interstitial Cystitis Mastitis Mittelschmerz Nephrolithiasis Nephrotic Syndrome Flare Nutcracker Syndrome Orchitis Ovarian Cyst Rupture Ovarian hyperstimulation syndrome Ovarian torsion Paraphimosis Pelvic Congestion Syndrome Pelvic Inflammatory Disease (PID)Peritoneal dialysis peritonitis Phimosis Priapism Prostatitis Pyelonephritis Renal laceration Renal transplant complications and rejection Ruptured ovarian cyst Testicular torsion Torsion of Appendix Testis Tubo-ovarian abscess Ureteral Rupture Urethritis Urinary Retention Urinary tract infection (uncomplicated)Urolithiasis (renal colic)Vaginal bleeding (non-pregnant)Vaginitis (Bacterial)Vaginitis (Candidal)Varicocele Vulvovaginal Hematoma

Infectious Disease Presentations148▾

Trauma Presentations89▾

Toxicologic Presentations80▾

Psychiatric Presentations26▾

Musculoskeletal and Rheumatologic Presentations96▾

Dermatology Presentations23▾

Environmental and Exposure Presentations27▾

Hematologic and Oncologic Presentations36▾

Pediatric-Specific Presentations19▾

Endocrine and Metabolic Presentations45▾

ENT and Maxillofacial Presentations27▾

Ophthalmologic Presentations19▾

Obstetric Presentations23▾

Systemic and Miscellaneous Presentations17▾

01Approach to the Critical Patient/attcp66

Immediate priorities

›Life-threatening complications of AKI

›Refractory hyperkalemia

›Peaked T waves on ECG

›Widened QRS or sine wave pattern

›If ECG changes, IV calcium immediately

›Severe metabolic acidosis

›pH < 7.20

›Bicarbonate < 12 mmol/l

›Refractory pulmonary edema

›Hypoxemia despite diuretics

›If unresponsive to medical therapy, emergent dialysis

›Uremic emergencies

›Encephalopathy

›Pericarditis

›Bleeding diathesis

›Hemodynamic and source threats

›Ongoing shock or sepsis

›SBP < 90 mmHg

›Lactate >= 2 mmol/l

›Sepsis as leading cause of ATN

›Most common ICU cause of severe AKI

›If septic, broad-spectrum antibiotics within 1 hour

›Volume depletion driving ischemic injury

›Hemorrhage

›Vomiting or diarrhea

›Early branching decision

›Prerenal vs intrinsic vs postrenal

02History/hx65

Presentation pattern

›Hallmark symptoms

›Oliguria or anuria

›Decreased urine output is the hallmark

›Nonoliguric in 30 to 40% especially nephrotoxic ATN

›Volume overload symptoms

›Edema

›Dyspnea or orthopnea

›Uremic symptoms

›Fatigue and nausea

›Confusion in advanced uremia

›Precipitating event context

›Recent hypotensive episode

›Surgery or ICU stay

›Hemorrhage or shock

›Nephrotoxin exposure

›Contrast within 48 to 72 hours

›New antibiotics or chemotherapy

›Pigment nephropathy clues

›Dark or cola-colored urine

›Crush injury or prolonged immobilization

Timing and tempo

›Onset relative to insult

›Ischemic ATN

›Develops 24 to 72 hours after insult

›Follows sustained hypoperfusion

›Aminoglycoside ATN

›Appears 5 to 10 days into therapy

03Physical Exam/exam37

Vitals and volume status

›Vital sign patterns

›Hypotension

›Ischemic ATN driver

›Tachycardia from hypovolemia

›Hypertension with pulmonary edema

›Volume overload state

›Crackles and elevated JVP

›Fever

›Sepsis or infection precipitant

›Volume status assessment as critical first step

›Hypovolemia signs

›Dry mucous membranes

›Flat JVP and orthostatic hypotension

›Hypervolemia signs

›Jugular venous distension

›Peripheral edema and S3 gallop

Organ-system findings

›Skin findings

›Livedo reticularis

›Suggests atheroembolic disease

›Blue toes with intact pulses

›Maculopapular rash

›Suggests acute interstitial nephritis

›Track marks

›Rhabdomyolysis from drug use

›Cardiopulmonary findings

›Pericardial friction rub

04Differential Diagnosis/ddx37

AKI category framework

›Prerenal azotemia

›Most common AKI cause overall

›FENa < 1%

›Urine osmolality > 500 mOsm/kg

›Responds to volume resuscitation

›Improvement within 24 to 48 hours

›ICD-10 N17.9 acute kidney failure unspecified

›Intrinsic AKI

›Acute tubular necrosis

›Muddy brown granular casts

›ICD-10 N17.0 acute kidney failure with tubular necrosis

›Acute interstitial nephritis

›Fever, rash, eosinophilia

›WBC casts; drug-related

›Glomerulonephritis

›RBC casts and dysmorphic RBCs

›Heavy proteinuria with FENa < 1%

›Postrenal obstruction

›Bilateral hydronephrosis

›BPH or pelvic malignancy

›ICD-10 N13.4 hydroureter

Dangerous mimics

›Hepatorenal syndrome

›AKI in cirrhosis

›FENa < 0.1% with bland sediment

›Responds to vasoconstrictors and albumin

›Diagnosis of exclusion

05Laboratory Tests/lt51

Renal function and electrolytes

›Basic metabolic panel

›Rising creatinine

›Diagnosis and KDIGO staging

›Compare to baseline value

›Elevated BUN

›BUN to creatinine ratio

›BUN > 112 mg/dL as nonurgent dialysis indication

›Hyperkalemia

›Most life-threatening complication

›Drives ECG and treatment urgency

›Low bicarbonate

›Metabolic acidosis severity

›Anion gap calculation

›Additional chemistry

›Phosphorus and uric acid

›Hyperphosphatemia in tubular injury

›Tumor lysis syndrome screen

›Calcium

›Hypocalcemia with hyperphosphatemia

›Hypercalcemia as AKI cause

Urine studies

›Urinalysis with microscopy

›Muddy brown granular casts

›Pathognomonic for ATN

›Tubular epithelial cells

›Cast differentiation

›RBC casts suggest glomerulonephritis

06Diagnostic Tests/dt65

Scoring Systems

›KDIGO AKI staging

›Stage 1

›Creatinine rise >= 0.3 mg/dL or 1.5 to 1.9x baseline

›Urine output < 0.5 mL/kg/h for 6 to 12 h

›Stage 2

›Creatinine 2.0 to 2.9x baseline

›Urine output < 0.5 mL/kg/h for >= 12 h

›Stage 3

›Creatinine >= 3x baseline or >= 4 mg/dL

›Need for renal replacement therapy

›Urine sediment scoring

›Sediment score >= 3

›Muddy brown casts and tubular cells

›High specificity for ATN

›Limitations

›Operator-dependent microscopy

›Clinical context required

›Novel biomarkers

›NGAL

›Predicts severe AKI

›May distinguish ATN from HRS

›TIMP-2 x IGFBP-7

›FDA-approved for AKI prediction

›Limited clinical availability

MRI

›MR role in AKI

›Limited acute utility

07Disposition/dispo30

Level of care

›Admission indications

›All new ATN

›Requires inpatient management

›Trend creatinine and electrolytes

›ICU indications

›Hemodynamic instability

›Need for renal replacement therapy

›Severe hyperkalemia with ECG changes

›Telemetry

›Moderate hyperkalemia K+ 6.0 to 6.5 mmol/l

›Pending treatment response

›Observation candidates

›Mild Stage 1 AKI

›Clear reversible cause such as NSAID use

›Creatinine trending down with stable electrolytes

›Close outpatient follow-up arranged

›Recheck within 1 to 2 weeks

Consultation and follow-up

›Nephrology consultation triggers

›Stage 3 AKI or unclear etiology

›Need for RRT

›Pre-existing CKD stage 4 or higher

›Inadequate response to supportive care

›Suspected glomerulonephritis or vasculitis

›Follow-up plan

›Recheck labs

›Creatinine and electrolytes within 1 to 2 weeks

08Treatment/t83

Initial stabilization

›Volume optimization

›Isotonic crystalloid for hypovolemia

›Balanced solution or normal saline

›Reassess after each bolus to avoid overload

›Diuretics for overload only

›Furosemide does not prevent or reverse ATN

›Used to manage volume, not improve renal outcome

›Remove the insult

›Discontinue nephrotoxins

›NSAIDs, ACE inhibitors, ARBs

›Aminoglycosides and contrast

›Treat underlying cause

›Antibiotics for sepsis

›Relieve obstruction

Hyperkalemia management

›Membrane stabilization

›Calcium gluconate IV

›1 to 2 g (10 to 20 mL of 10%) over 2 to 3 minutes

›Repeat if ECG changes persist

›Onset within minutes, short duration

›Intracellular potassium shift

›Insulin with dextrose

›Regular insulin 10 units IV

›Dextrose 25 g IV if glucose < 14 mmol/l

›Monitor for hypoglycemia

›Nebulized albuterol

›10 to 20 mg nebulized

09Special Populations/sp39

Pregnancy

›Pregnancy-specific considerations

›Causes unique to pregnancy

›Preeclampsia and HELLP

›Pregnancy-related TMA

›Physiologic baseline

›GFR increased; normal creatinine is lower

›Creatinine > 0.8 mg/dL may be abnormal

›Medication safety

›Avoid ACE inhibitors and ARBs

›Avoid NSAIDs especially third trimester

›Dialysis approach

›More frequent dialysis with lower BUN targets

›Maternal-fetal monitoring

Geriatric

›Older adult features

›Reduced renal reserve

›Lower baseline GFR

›Creatinine underestimates dysfunction with low muscle mass

›Polypharmacy risk

›Multiple nephrotoxins

›Careful medication reconciliation

›Volume sensitivity

›Prone to both depletion and overload

›Cautious fluid titration

›Atypical presentation

›Delirium as presenting sign

›Higher mortality and non-recovery risk

10Background/b51

Epidemiology

›Burden and causes

›ATN is most common intrinsic AKI cause

›Ischemic or nephrotoxic tubular injury

›Frequently diagnosed presumptively

›Sepsis predominates in ICU

›47% of severe AKI cases

›Major contributor to mortality

›Nephrotoxic exposure

›22% of inpatient AKI meets nephrotoxic criteria

›Recurrent AKI in 25% within 12 months

›Outcomes

›Recovery

›Over 85% with previously normal kidneys recover within 6 to 12 months

›Oliguric ATN has worse prognosis than nonoliguric

›Mortality

›In-hospital mortality ~50% in severe cases needing RRT

›Driven largely by underlying illness

Pathophysiology

›Mechanisms of tubular injury

›Ischemic injury

›Sustained hypoperfusion

›Tubular epithelial cell death and sloughing

›Nephrotoxic injury

›Direct tubular toxicity

›Aminoglycosides, contrast, cisplatin

›Pigment nephropathy

›Myoglobin or hemoglobin tubular obstruction

11Patient Discharge Instructions/pdi20

copy discharge instructions

›Acute kidney injury home care

›Take only medications approved by your kidney team

›Avoid ibuprofen, naproxen, and other anti-inflammatory drugs

›Stay hydrated unless told to limit fluids

›Follow any low-potassium and low-salt diet instructions

›Warning signs to return to ER

›Little or no urine output

›Swelling of legs or face or sudden weight gain

›Shortness of breath

›Confusion or excessive drowsiness

›Nausea or vomiting preventing you from drinking

›Chest pain or palpitations

›Follow-up

›Blood test to recheck kidney function within 1 to 2 weeks

›Kidney specialist appointment as arranged

›Bring an updated list of all medications

›Long-term kidney protection

›Tell every provider about your AKI history

›Ask about hydration before any contrast scan

›Keep blood pressure and diabetes well controlled

12References/r15

Guidelines and key sources

›Major guidelines

›KDIGO Clinical Practice Guideline for Acute Kidney Injury

›ACR Manual on Contrast Media 2025

›VA DoD Primary Care Management of CKD 2025

›Landmark trials on dialysis timing

›STARRT-AKI trial NEJM 2020

›AKIKI and IDEAL-ICU trials

›Watchful waiting non-inferior to early RRT

›Key reviews and evidence

›Ostermann et al, Acute Kidney Injury, Lancet 2025

›Abdelhafez et al, FENa diagnostic performance meta-analysis CJASN 2022

›Cochrane reviews on diuretics and fenoldopam for AKI

›Coding standards

›ICD-10 N17.0 acute kidney failure with tubular necrosis

›SNOMED CT acute tubular necrosis disorder concept

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Reviewed by SymptomDx Medical Team · Last reviewed August 18, 2026

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