Genitourinary Renal System

Acute Kidney Injury (AKI) and Related Renal Conditions

  • AKI definition: abrupt or rapid decline in kidney function resulting in waste retention and dysregulation of volume status and electrolytes; often prerenal causes and acute tubular necrosis (ATN) are most common etiologies; KDIGO staging defines AKI and its criteria.

  • KDIGO AKI criteria:

    • Increase in serum creatinine by at least 0.3\,\text{mg/dL} within 48 hours, or

    • Increase in serum creatinine by at least \geq 1.5\times baseline within the prior 7 days, or

    • Urine volume < 0.5\,\text{mL/kg/hr} for 6 hours.

  • Typical AKI course: may last about 7-21\text{ days}; some recover in days, others require dialysis for months.

  • Common etiologies and categories:

    • Prerenal (hypoperfusion) due to volume depletion, decreased cardiac output, or renal hypoperfusion states; often reversible with rehydration.

    • Intrarenal (ATN, acute interstitial nephritis, glomerular disease) involving parenchyma or tubules; ATN causes ~90% of intrinsic AKI and is often reversible.

    • Postrenal (obstruction) due to bladder outlet or ureteral/renal obstruction; bilateral obstruction or single kidney with obstruction can cause AKI.

  • KDIGO staging for AKI is distinct from CKD staging and guides management and prognosis.

Normal Findings: Kidneys and Urinary System

  • Location: retroperitoneal; right kidney sits lower than left due to liver displacement.

  • Basic functional units: nephrons (contain glomeruli).

  • Kidney roles:

    • Regulate electrolytes and fluids to influence blood pressure.

    • Water reabsorption influenced by antidiuretic hormone (ADH) and aldosterone.

    • Excretion of water-soluble wastes (e.g., creatinine, urea, uric acid).

    • Hormone secretion:

    • Erythropoietin (RBC production)

    • Renin and bradykinin (blood pressure)

    • Prostaglandins (renal perfusion)

    • Calcitriol (vitamin D3) for bone health

  • Average daily urine output: \approx 1500\,\text{mL}.

  • Oliguria definition: urine output < 400-500\,\text{mL/day} in adults.

Laboratory Testing: Key Markers and Indices

Serum Creatinine

  • Creatinine source: product of creatine metabolism in skeletal muscle and from dietary meat intake.

  • Normal values differ by sex due to muscle mass:

    • Males: 0.7-1.3\,\text{mg/dL}

    • Females: 0.6-1.1\,\text{mg/dL}

  • When renal function declines, serum creatinine rises; creatinine may be falsely low with low muscle mass (e.g., older adults).

  • Serum creatinine levels vary inversely with GFR.

Creatinine Clearance (24-hour urine)

  • Used to evaluate proteinuria/albuminuria/microalbuminuria and to reflect renal function over a 24-hour period.

  • Characteristics:

    • More sensitive than serum creatinine alone for certain assessments.

    • Relatively constant and not affected by fluid status, diet, or exercise.

    • Creatinine clearance roughly doubles for every 50% reduction in GFR.

  • Practical note: ideally, exercise should be avoided immediately before and during specimen collection.

Estimated Glomerular Filtration Rate (eGFR)

  • eGFR is the best overall test to measure kidney function and to stage CKD (per KDIGO).

  • Normal eGFR: >90\,\text{mL/min}.

  • CKD defined as eGFR < 60 for at least 3 months (with or without kidney damage).

  • eGFR calculation:

    • Based on serum creatinine, age, and sex.

    • Two common equations used historically: Modification of Diet in Renal Disease (MDRD) and CKD-EPI (2009).

    • 2021 CKD-EPI equation is now recommended and was developed without a race coefficient.

  • GFR factors:

    • Age-related decline with age

    • Sex differences due to muscle mass

    • Body size

    • Some patients with underlying kidney disease may have a normal eGFR; eGFR can be less reliable in pregnancy, muscle wasting, elderly patients, and lower-extremity amputees.

  • Tips:

    • eGFR is considered the best overall measure of renal function in primary care.

    • Serum creatinine is a better measure of renal function than BUN or BUN/Cr ratio for many purposes.

Blood Urea Nitrogen (BUN)

  • BUN reflects the liver's conversion of amino acids to ammonia, than urea; assesses kidneys’ ability to excrete urea.

  • BUN can rise with kidney damage or decreased renal blood flow; it is less sensitive than creatinine or eGFR.

  • Urea production is not constant—can increase with high-protein diet, tissue breakdown (hemorrhage, trauma, glucocorticoids).

  • Low-protein diet or liver disease can lower BUN without affecting GFR.

  • In heart failure, lower GFR with higher BUN correlates with higher mortality; in ICU, elevated BUN is independently associated with mortality.

BUN-to-Creatinine Ratio (BUN:Cr)

  • A rise in the BUN:Cr ratio suggests decreased kidney perfusion (prerenal state).

  • Used to help classify prerenal, infrarenal, or postrenal etiologies of AKI.

Urinalysis (UA) with Microscopic Exam

A complete UA includes gross evaluation, dipstick analysis, and microscopic urine sediment.

  • Epithelial cells:

    • Large amounts of squamous epithelial cells indicate contamination (normal to have a few).

    • Squamous cells from external urethra; transitional epithelial cells from the bladder.

  • White Blood Cells (Leukocytes):

    • Normal WBCs in urine: ≤2-5 WBCs/hpf (high-power field).

    • Leukocyte esterase indicates presence of WBCs.

    • Presence of neutrophils commonly associated with bacteria.

    • Leukocytes in urine (pyuria) almost always present in acute cystitis in males.

  • Red Blood Cells:

    • Few RBCs (<3 cells) considered normal.

    • Microscopic hematuria = RBCs visible only on microscopy.

    • Gross hematuria = visible blood in urine; color ranges pink/red/cola/brown; bleeding may originate from urethra (urethritis), bladder (cystitis or cancer), or kidneys (stones, pyelonephritis, PKD, cancer).

    • Contamination possible from menses, vaginal discharge, semen, hemorrhoids, rectal bleeding.

  • Protein:

    • Persistent protein suggests chronic kidney damage; assess serum creatinine and eGFR; request urine for microscopy.

    • Isolated proteinuria = proteinuria with normal kidney function and stable sediment.

    • Transient proteinuria common in patients ≤18 years or young adults; diagnosed if repeat test becomes negative.

    • Benign causes include fever, intense physical activity, acute illness, dehydration, emotional stress; may be present in acute pyelonephritis (resolves after treatment).

    • Urine dipsticks are sensitive to albumin; false positives can occur with alkaline urine (pH > 7.5), excessive immersion, concentrated urine, gross hematuria, semen, or vaginal secretions.

    • For quantification, order 24-hour urine protein or protein-to-creatinine ratio (UPr/Cr).

  • Nitrites:

    • Bacteria reduce urinary nitrate to nitrite; positive nitrite is highly indicative of a UTI.

  • Casts:

    • Cylindrical structures formed in renal tubules.

    • Hyaline casts: nonspecific; seen with low urine volumes or diuretic therapy.

    • Granular casts: protein or other debris suggestive of infection or inflammation.

    • WBC casts: seen with infection (pyelonephritis) or interstitial nephritis.

    • RBC casts: suggest glomerular bleeding (glomerulonephritis) with edema, dark urine, hypertension.

  • Urine pH:

    • Reference range: 4.5 to 8.0; useful for evaluating stones and infections.

    • Diet effects: citrus/low-carb diets lower acidity; high-protein diets raise acidity.

  • Urine Culture and Sensitivity (C&S):

    • Confirms bacteriuria and identifies antibiotic susceptibility.

    • Specimen: clean-catch voided sample for suspected UTI.

    • Positive culture: ≥ 10^5 CFU/mL of one dominant organism.

    • If multiple organisms: sample may be contaminated; lower values may still indicate bacteriuria.

  • Tips:

    • Interpret UA results in the context of UTI.

    • WBC casts with proteinuria and hematuria are associated with pyelonephritis.

Chronic Kidney Disease (CKD) Stages

  • Stage I: GFR \ge 90 mL/min; Kidney damage with normal or high kidney function.

  • Stage II: GFR 60-89 mL/min; Mild loss of kidney function.

  • Stage IIIa: GFR 45-59; Mild-to-moderate loss.

  • Stage IIIb: GFR 30-44; Moderate-to-severe loss.

  • Stage IV: GFR 15-29; Severe loss.

  • Stage V: GFR < 15 mL/min; Kidney failure.

Acute Kidney Injury: Causes, Staging, and Management

  • AKI is an abrupt reduction in GFR with waste retention and electrolyte/volume dysregulation.

  • Common presentations include oliguria, edema, weight gain, lethargy, nausea, malaise.

  • KDIGO AKI staging criteria (as above) are used to define and stage AKI.

  • Pre-renal causes: due to hypoperfusion

  • Intrinsic renal causes: include ATN, nephrotoxic drugs, glomerular diseases; ATN accounts for the majority of intrinsic AKI and is often reversible.

  • Post-renal causes: obstruction within the urinary tract; obstruction commonly bilateral or in a patient with single functioning kidney.

  • General management:

    • Early nephrology and ED referral when indicated.

    • Dialysis emergently for hypervolemia with pulmonary edema, severe hyperkalemia, life-threatening uremic symptoms, or toxin exposure.

    • Remove nephrotoxic insults, correct hypovolemia, correct electrolyte abnormalities and acidosis, provide nutrition management (potassium, phosphorus, fluid limits).

  • Nephrotoxic drugs include (examples):

    • Acyclovir, allopurinol, aminoglycosides, certain antivirals, beta-lactams, chemotherapy agents, contrast dyes, diuretics, illicit drugs, lithium, NSAIDs/analgesics, proton pump inhibitors, quinolones, sulfonamides, and others.

  • AKI etiologies by category (summary):

    • Pre-renal: hypovolemia, decreased cardiac output, third-space sequestration (sepsis, pancreatitis, hypoalbuminemia), medications limiting GFR (ACE inhibitors, ARBs, NSAIDs).

    • Post-renal: bladder obstruction (BPH, cancer), urethral/renal obstruction (stones, strictures, clots, cancer), neurogenic bladder.

    • Intra-renal: ATN (ischemia/hypoperfusion/sepsis/hemorrhage/nephrotoxins); drugs such as NSAIDs, diuretics, penicillins, cephalosporins, sulfa drugs, allopurinol, anticoagulants; glomerular diseases; thrombosis of renal vessels.

Acute Pyelonephritis

  • Acute bacterial infection of the kidneys; most commonly caused by gram-negative Enterobacteriaceae (E. coli 75-95%, Proteus, Klebsiella).

  • Outpatient treatment suitable for compliant, healthy patients with milder disease (uncomplicated):

    • Oral fluoroquinolones (e.g., levofloxacin or ciprofloxacin) for 5-7 days.

  • Complicated/Severe disease or immunocompromised patients require hospitalization for rehydration and management of complications; refer for inpatient care.

  • Classic case: high fever, chills, anorexia, nausea/vomiting, unilateral flank pain; may have cystitis symptoms (dysuria, frequency, urgency).

  • Diagnostic criteria and tests:

    • Temperature ≥ 100.4\,\text{°F} (≥ 38.0 °C)

    • Costovertebral angle tenderness

    • Urinalysis: leukocytes, hematuria, nitrites, mild proteinuria

    • Urine casts: WBC casts on microscopic exam

    • Urine culture and sensitivity: ≥ 10^5\,\text{CFU/mL} of one organism

    • CBC: leukocytosis, neutrophilia with left shift (bands) suggesting infection

    • Chemistry panel including serum creatinine

  • Pregnancy, children/elderly, male patients, kidney stones, anatomic abnormalities, diabetes, and immunocompromise require specialist referral.

  • Management tips:

    • Distinguish classic acute simple cystitis vs. acute pyelonephritis.

    • Monitor for progression to bacteremia/sepsis, and adjust therapy if needed.

Asymptomatic Bacteriuria (ASB)

  • Defined as presence of one or more bacterial species in urine at ≥ 10^5\,\text{CFU/mL} without UTI symptoms.

  • Prevalence:

    • Healthy females: increases with age, from ~1% to >20% after age 80.

    • Diabetics: 8-14% prevalence.

    • Males >75 years: 6-15%.

  • Treatment indications:

    • Pregnancy, patients undergoing urologic intervention, renal transplant recipients.

  • Screening/treatment not recommended for older patients, diabetics, indwelling catheters, or those undergoing non-urologic surgery.

Chronic Kidney Disease (CKD) Overview

  • CKD definition: presence of kidney damage (structural or functional abnormalities) or GFR <60ml/min/1.73for 3+ months, regardless of cause.

  • Common etiologies: poorly controlled diabetes mellitus and hypertension.

  • CKD staging is based on GFR.

  • Classic CKD presentation: edema from fluid overload or hypertension; fatigue, weakness, anorexia, vomiting, pruritus; advanced disease may cause encephalopathy or seizures.

  • Physical findings:

    • Volume overload: weight gain, edema, shortness of breath

    • Volume depletion signs in other contexts: fatigue, postural dizziness, tachycardia, dry skin

    • Possible findings: rashes, skin lesions, abnormal bruits or distal pulses (renal artery stenosis), enlarged kidneys (polycystic disease), peripheral neuropathy with diabetic disease

  • Laboratory features:

    • Serum creatinine and BUN often elevated; eGFR decreased; proteinuria/albuminuria may be present on urine microscopy

    • CBC may show anemia; metabolic derangements such as hyperkalemia, hyperphosphatemia, metabolic acidosis, hypocalcemia, elevated PTH

    • Urine studies may show proteinuria/albuminuria and possibly RBCs/WBCs

    • Random protein-to-creatinine ratio and albumin-to-creatinine ratio quantify protein/albuminuria

  • Diagnostics:

    • CBC with differential

    • Basic metabolic panel

    • Urinalysis with microscopy

    • Kidney ultrasound to assess structural abnormalities; vascular duplex ultrasound to evaluate renal artery stenosis

  • Management:

    • May require dialysis in some patients; trajectory and duration determine therapy needs

    • Nephrology consult for advanced disease (eGFR <30mL/min/1.73, persistent high proteinuria, etc.)

  • Diet and education:

    • Nutritional support tailored to eGFR and comorbidities; DASH diet is a common reference diet for renal patients

Hematuria: Types, Evaluation, and Implications

  • Two types:

    • Microscopic hematuria: RBCs detectable only on microscopy (≥3 RBCs/hpf sometimes used as threshold)

    • Gross (visible) hematuria: pink/red/brown urine; may contain clots

  • Possible sources include urethra, bladder, prostate, kidneys (pyelonephritis, stones, cancer, PKD)

  • Diagnostic approach:

    • UA with microscopy; if infection suspected, assess leukocytes and nitrites

    • Consider urine cytology if urothelial malignancy suspected (risk factors include age >50, male sex, smoker, gross hematuria)

    • In gross hematuria with clots or persistent bleeding, imaging and nephrology/urology referral

  • Post-infectious hematuria considerations: new dark urine after strep infection suggests possible poststreptococcal glomerulonephritis (PSGN), common in children; onset 10 days to 3 weeks after infection

Glomerular and Renal Bleeding Syndromes

  • Glomerular bleeding may yield gross hematuria without clots; consider glomerulonephritis.

  • Hematuria workup may include imaging and nephrology referral when glomerular disease is suspected.

Nephrolithiasis (Renal Calculi)

  • Stone composition:

    • Calcium oxalate: 70-80%

    • Calcium phosphate: ~15%

    • Struvite: ~1%

    • Uric acid: ~8%

    • Cystine: 1-2%

  • More common in males; prevalence increases with age.

  • Pain presentation depends on stone location and size; renal pelvis or upper tract stones cause flank pain; distal stones cause abdominal pain and may radiate to genitals.

  • Risk factors for calcium stones:

    • Urinary factors: low volume, high calcium, high oxalate, low citrate, high urine pH

    • Anatomic: horseshoe kidney, medullary sponge kidney

    • Diet: high calcium/oxalate, high sodium and protein intake, low fluids, high sucrose/fructose

    • Other conditions: obesity, diabetes, gout, IBD, post-bariatric surgery

    • Non-modifiable: family history, genetics, White race

  • Classic case: sudden colicky flank pain on one side with waves; may have nausea/vomiting; most stones pass spontaneously within 48 hours in many cases; gross or microscopic hematuria common.

  • Diagnostics:

    • UA often shows hematuria; microscopy may show crystals depending on stone type

    • CT abdomen/pelvis without contrast is the preferred imaging modality; ultrasound alternatives in pregnancy or if CT unavailable

  • Management:

    • Most stones managed conservatively with analgesia and hydration if the patient tolerates PO intake and fluids

    • Stones ≤ 5 mm largely pass spontaneously; advise patient to strain urine and bring passed stone for analysis

    • Stones 5-10 mm: consider tamsulosin (or other alpha-blocker) for up to 4 weeks to facilitate passage; calcium channel blockers may also be used

    • Pain control: NSAIDs (e.g., indomethacin, ketorolac) and/or opioids; NSAIDs may reduce ureteral spasm but can worsen AKI risk in dehydration or CKD

    • Stones > 10 mm or failed medical expulsive therapy, urology consult; larger stones may require ESWL (extracorporeal shock wave lithotripsy) or other interventions

    • Indications for ED referral include fever (possible urosepsis), persistent severe pain, AKI, anuria, inability to tolerate oral medications, or large stones

  • Diet and prevention:

    • Increase fluids to 2-3 L/day

    • For calcium oxalate stones, limit high-oxalate foods (rhubarb, spinach, okra, nuts, beets, chocolate, tea, some meats)

Proteinuria: Types, Evaluation, and Implications

  • Definition: excretion of >150\,\text{mg/day} of protein.

  • Proteinuria as a marker of kidney damage; persistent proteinuria warrants etiologic investigation.

  • Four major types:

    • Glomerular, tubular, overflow, postrenal

  • Assessment:

    • Gold standard: 24-hour urine collection for protein excretion

    • Urine dipstick detects albumin poorly at low levels; microalbuminuria may be missed without concentration; repeat testing may be needed.

  • Transient proteinuria: common in fever, exercise, acute illness, dehydration, emotional stress; if transient, repeat test may be negative.

  • False positives and confounders: fever, dehydration, etc., may affect results; persistent or significant proteinuria requires further workup.

Urinary Tract Infections (UTIs)

  • Cystitis (bladder inflammation) can be uncomplicated, recurrent, reinfection, or relapse; most UTIs are due to Enterobacteriaceae (E. coli, Klebsiella, etc.).

  • Common pathogens and risk groups:

    • Infants: UTIs common in boys in first 6 months due to anatomical issues.

    • Children: UTIs require evaluation; ~2.5% of children get a UTI; may indicate vesicoureteral reflux or risk of abuse.

    • Females: Highest incidence during reproductive years.

    • Older females: New urinary symptoms or incontinence can indicate UTI.

  • Risk factors:

    • Female sex, pregnancy, recent UTI history, diabetes/immunocompromised, postcoital UTI, poor hydration, catheterization, use of spermicides (nonoxynol-9) increasing risk of UTIs.

  • Classic female UTI case: dysuria, frequency, urgency, nocturia; suprapubic discomfort; UA shows leukocytes and nitrites; urine culture may be positive.

  • Diagnosis and testing:

    • UA dipstick: leukocyte esterase; nitrites; WBCs; hematuria; pH; possibly protein.

    • Urine culture (C&S): commonly >= 10^5\,\text{CFU/mL} of a single organism; mixed flora may indicate contamination.

    • In uncomplicated cystitis in healthy females, UA alone may suffice; C&S not routinely required.

  • Acute simple cystitis in healthy adult females (outpatients): First-line antibiotics include

    • Nitrofurantoin 100\,\text{mg} twice daily for 5\text{ days}; trimethoprim-sulfamethoxazole (TMP-SMX) 160/800\,\text{mg} twice daily for 3\text{ days}; fosfomycin single dose 3\,\text{g}; pivmecillinam 400 mg orally three times daily for 3-5 days (some guidelines vary by region).

  • Special considerations:

    • For patients at risk of resistant organisms, options include nitrofurantoin, fosfomycin, pivmecillinam; fluoroquinolones may be used in certain resistant cases but have higher risk of resistance and adverse effects.

    • Phenazopyridine (Pyridium) is a urinary analgesic for symptomatic relief; it colors urine orange and can stain contact lenses; avoid in liver/kidney disease or G6PD deficiency; not curative.

    • Fluid intake: increase to 2-3 L/day; dietary oxalate restriction advised in stone-formers, not specifically required for all simple cystitis.

  • Recurrent UTIs in females:

    • Defined as three or more culture-positive UTIs in 1 year or two UTIs within 6 months.

    • Antibiotic prophylaxis is not first-line therapy.

    • Postcoital prophylaxis options include nitrofurantoin, TMP-SMX, cephalexin; advise hydration and avoid spermicides; estrogen therapy may be used in postmenopausal women; cranberry products and probiotics lack demonstrated efficacy.

  • Acute simple cystitis in adult males:

    • Less common; evaluate for underlying structural issues (urethral stricture, BPH, calculi, uncircumcised status).

    • Management similar to females but with broader differential including STI testing (NAAT for gonorrhea and chlamydia).

  • Pearls and cautions:

    • Do not routinely screen or treat ASB in most populations except indicated groups (e.g., pregnancy).

    • Avoid prolonged nitrofurantoin use due to risk of lung, hepatic, and neuropathic toxicity; monitor in patients with CKD.

    • ACE inhibitors/ARBs require potassium monitoring in patients with CKD due to risk of hyperkalemia.

    • Contrast media can cause contrast-associated AKI; higher risk in CKD or diabetes; minimize exposure when possible.

Acute Simple Cystitis in Males and Special Considerations

  • In adult males, assess for structural/anatomic causes (urethral stricture, BPH, stones, uncircumcised) and potential STI involvement; treat with nitrofurantoin, TMP-SMX, or fosfomycin as appropriate; evaluate for recurrent infections and refer to urology if needed.

  • Long-term nitrofurantoin use is associated with lung problems, chronic hepatitis, and neuropathy; baseline tests (chest X-ray, LFTs) and monitoring advised; contraindicated in renal insufficiency.

Urinary Tract Imaging and Procedures

  • Imaging preferences:

    • Noncontrast CT scan is the highest sensitivity/specificity for kidney stones.

    • Ultrasound can be used when CT is unavailable or if patient is pregnant.

  • Urine cytology and cystoscopy considerations in suspected malignancy or persistent hematuria with risk factors.

Practical Tips and Educational Highlights

  • eGFR is the best single measure of renal function in primary care; use eGFR for CKD staging and progression monitoring.

  • Serum creatinine alone can be misleading in certain populations (older adults, low muscle mass); use eGFR and creatinine clearance when appropriate.

  • BUN/Cr ratio helps classify prerenal vs intrinsic renal disease and guides management.

  • Urinalysis interpretation should consider contamination, pyuria, nitrite positivity, leukocyte esterase, casts, and hematuria patterns to differentiate UTI, pyelonephritis, and glomerular/glomerulonephritis processes.

  • In AKI, rapid identification of prerenal causes and avoidance of nephrotoxins are essential, followed by careful fluid and electrolyte management.

  • For stone prevention, appropriate hydration and dietary modifications depend on stone type; oxalate-rich foods should be moderated for calcium oxalate stones.

  • DASH diet is a common dietary framework for CKD-related nutrition planning; nutrition should be individualized based on eGFR and comorbidities.

  • Education on recognizing symptoms, appropriate timing of imaging, and when to seek ED or specialist care is critical for AKI and CKD management.

Equations and Numerical References (LaTeX)

  • KDIGO AKI criteria:

    • \Delta Cr \ge 0.3\,\text{mg/dL} \text{within } 48\text{ hours}

    • \Delta Cr \ge 1.5 \times \text{baseline within 7 days}

    • \text{Urine output} < 0.5\,\frac{\text{mL}}{\text{kg}\cdot \text{hr}} \text{for } 6\text{ hours}

  • eGFR normal threshold: \text{eGFR} > 90\,\text{mL/min}

  • CKD staging GFR cutoffs:

    • Stage I: \text{GFR} \ge 90\quad\text{mL/min} (kidney damage with normal/high function)

    • Stage II: 60 \le \text{GFR} \le 89\quad\text{mL/min}

    • Stage IIIa: 45 \le \text{GFR} \le 59\quad\text{mL/min}

    • Stage IIIb: 30 \le \text{GFR} \le 44\quad\text{mL/min}

    • Stage IV: 15 \le \text{GFR} \le 29\quad\text{mL/min}

    • Stage V: \text{GFR} < 15\quad\text{mL/min}

  • Urine culture thresholds:

    • Positive culture: \ge 10^5\ \text{CFU/mL} of one dominant organism.

  • Proteinuria threshold (excretion):

    • > 150\ \text{mg/day} of protein.

References to Clinical Scenarios and Tables (Conceptual)

  • Classic cases described throughout the notes illustrate AKI, AKI etiologies, pyelonephritis, CKD progression, ASB management, UTI management, nephrolithiasis management, and urinary laboratory interpretation.

  • Use based on KDIGO definitions, eGFR-based CKD staging, and guideline-consistent antibiotic options for uncomplicated cystitis and pyelonephritis, with attention to resistance risks and patient comorbidities.