const pptxgen = require('pptxgenjs');

let pptx = new pptxgen();
pptx.layout = 'LAYOUT_WIDE';
pptx.author = 'Orris';
pptx.title = 'Acute Kidney Injury (AKI)';
pptx.subject = 'Residents/Postgraduates';
pptx.company = 'Medical Education';
pptx.lang = 'en-US';

const TITLE_COLOR = '0B1F3A';
const ACCENT = '0E7490';
const TEXT = '1F2937';
const BG = 'F8FAFC';

function addTitle(slide, title, subtitle='') {
  slide.background = { color: BG };
  slide.addText(title, { x: 0.4, y: 0.2, w: 12.4, h: 0.6, fontSize: 28, bold: true, color: TITLE_COLOR, fontFace: 'Calibri' });
  if (subtitle) {
    slide.addText(subtitle, { x: 0.4, y: 0.85, w: 12.4, h: 0.35, fontSize: 14, color: ACCENT, fontFace: 'Calibri' });
  }
  slide.addShape(pptx.ShapeType.line, { x: 0.4, y: 1.2, w: 12.4, h: 0, line: { color: 'CBD5E1', pt: 1 } });
}

function addBullets(slide, items) {
  const lines = [];
  items.forEach((it, idx) => {
    lines.push({ text: it, options: { bullet: { indent: 18 }, breakLine: idx < items.length - 1 } });
  });
  slide.addText(lines, { x: 0.7, y: 1.45, w: 12.0, h: 5.7, fontSize: 20, color: TEXT, fontFace: 'Calibri', valign: 'top', margin: 4, paraSpaceAfterPt: 10 });
}

function addRef(slide, ref) {
  slide.addText(ref, { x: 0.5, y: 6.85, w: 12.0, h: 0.35, fontSize: 10, color: '475569', italic: true, align: 'right', fontFace: 'Calibri' });
}

let s;

s = pptx.addSlide();
s.background = { color: 'E2E8F0' };
s.addText('Acute Kidney Injury (AKI)', { x: 0.8, y: 1.8, w: 11.7, h: 0.9, fontSize: 42, bold: true, color: TITLE_COLOR, align: 'center' });
s.addText('Comprehensive Review for Residents/Postgraduates', { x: 1.2, y: 2.8, w: 10.9, h: 0.6, fontSize: 22, color: ACCENT, align: 'center' });
s.addText('Reference: Harrison\'s Principles of Internal Medicine (latest available edition)', { x: 1.0, y: 6.4, w: 11.2, h: 0.4, fontSize: 12, color: '334155', align: 'center', italic: true });

s = pptx.addSlide();
addTitle(s, 'Learning Objectives');
addBullets(s, [
  'Define AKI and apply KDIGO staging criteria accurately in clinical settings',
  'Differentiate prerenal, intrinsic, and postrenal AKI using history, exam, and urine indices',
  'Develop a practical diagnostic algorithm for oliguric and non-oliguric AKI',
  'Implement evidence-based management, including fluid, electrolyte, and RRT decisions',
  'Recognize prevention strategies for hospital-acquired AKI and contrast-associated injury'
]);
addRef(s, 'Harrison\'s Principles of Internal Medicine, latest ed.');

const slides = [
  ['Definition of AKI', [
    'AKI is a rapid decline in kidney excretory function over hours to days',
    'Operational criteria include rise in serum creatinine and/or reduction in urine output',
    'Creatinine rise often lags behind injury; oliguria may be an earlier marker',
    'AKI is a clinical syndrome with heterogeneous etiologies and outcomes'
  ]],
  ['KDIGO Diagnostic Criteria and Staging', [
    'Stage 1: SCr 1.5-1.9 × baseline or e0.3 mg/dL rise; urine <0.5 mL/kg/h for 6-12 h',
    'Stage 2: SCr 2.0-2.9 × baseline; urine <0.5 mL/kg/h for e12 h',
    'Stage 3: SCr e3 × baseline or e4.0 mg/dL, or need for RRT; severe oliguria/anuria',
    'Always stage by the worst of creatinine or urine output criteria'
  ]],
  ['Epidemiology and Clinical Burden', [
    'AKI occurs in about 20-25% of hospitalized adults; higher in ICU populations',
    'Associated with prolonged hospitalization, higher costs, and increased mortality',
    'Even transient AKI increases risk of CKD progression and long-term cardiovascular events',
    'Early identification and prevention are key quality-of-care targets'
  ]],
  ['AKI Phenotypes by Site/Mechanism', [
    'Prerenal AKI: reduced effective renal perfusion without initial structural damage',
    'Intrinsic AKI: tubular, interstitial, glomerular, or vascular injury',
    'Postrenal AKI: urinary tract obstruction with back pressure and reduced GFR',
    'Mixed phenotypes are common in critically ill patients'
  ]],
  ['Pathophysiology: Hemodynamics and Cellular Injury', [
    'Reduced perfusion activates RAAS, sympathetic tone, and ADH with sodium/water retention',
    'Ischemia and toxins cause tubular epithelial injury, polarity loss, and cell death',
    'Microvascular dysfunction and inflammation amplify ongoing kidney damage',
    'Repair may be adaptive (recovery) or maladaptive (fibrosis, CKD transition)'
  ]],
  ['Common Causes of Prerenal AKI', [
    'True volume depletion: GI losses, hemorrhage, burns, osmotic diuresis',
    'Reduced effective arterial volume: heart failure, cirrhosis, sepsis',
    'Hemodynamic drugs: NSAIDs (afferent constriction), ACEI/ARB (efferent dilation)',
    'Renal hypoperfusion may progress to ischemic tubular injury if prolonged'
  ]],
  ['Intrinsic AKI: Major Categories', [
    'Acute tubular injury/necrosis (ischemic or nephrotoxic) is most common',
    'Acute interstitial nephritis, often drug-induced (antibiotics, PPIs, NSAIDs)',
    'Glomerulonephritis and vasculitic disorders cause inflammatory renal injury',
    'Vascular causes include thrombotic microangiopathy, emboli, malignant hypertension'
  ]],
  ['Postrenal AKI: Obstructive Etiologies', [
    'Bladder outlet obstruction: prostatic hypertrophy, urethral pathology',
    'Ureteric obstruction: stones, malignancy, fibrosis, clots, external compression',
    'Consider obstruction in oliguria/anuria and in high-risk cancer/urologic patients',
    'Rapid relief often leads to substantial renal recovery'
  ]],
  ['History and Examination in AKI', [
    'Assess recent volume losses, sepsis, surgery, hypotension, nephrotoxin exposure',
    'Review medication timeline including OTC NSAIDs and herbal preparations',
    'Evaluate fluid status: orthostasis, JVP, edema, perfusion markers',
    'Look for clues to systemic disease: rash, arthritis, hemoptysis, livedo'
  ]],
  ['Initial Laboratory Workup', [
    'Trend serum creatinine, BUN, electrolytes, bicarbonate, calcium, phosphate',
    'Urinalysis and urine microscopy are high-yield early tests',
    'Quantify urine output accurately with nursing charts/catheter data',
    'Use blood gas when acidosis or respiratory compromise is suspected'
  ]],
  ['Urinalysis Patterns that Localize AKI', [
    'Prerenal: bland sediment or hyaline casts',
    'Tubular injury: muddy brown granular casts, renal tubular epithelial cells',
    'AIN: pyuria, WBC casts, mild proteinuria, eosinophiluria (limited sensitivity)',
    'GN: hematuria, dysmorphic RBCs, RBC casts, significant proteinuria'
  ]],
  ['Urine Indices: FENa and FEUrea', [
    'FENa <1% favors prerenal states in oliguric patients not on diuretics',
    'FENa >1-2% suggests tubular injury but has context-specific limitations',
    'FEUrea may be useful when diuretics confound sodium handling',
    'Always interpret indices alongside clinical context and microscopy'
  ]],
  ['Imaging in AKI', [
    'Kidney-bladder ultrasound is first-line to exclude hydronephrosis/retention',
    'Doppler studies when renal vascular compromise is suspected',
    'Avoid unnecessary contrast studies in high-risk AKI unless clinically imperative',
    'Point-of-care ultrasound can assist dynamic fluid assessment'
  ]],
  ['Biomarkers Beyond Creatinine', [
    'Tubular stress/injury markers include NGAL, KIM-1, IL-18, TIMP2-IGFBP7',
    'Potential role in early risk stratification before overt creatinine rise',
    'Current real-world use is variable due to availability and interpretation challenges',
    'Biomarkers complement but do not replace clinical assessment'
  ]],
  ['General Principles of AKI Management', [
    'Treat underlying cause while providing meticulous supportive care',
    'Stop nephrotoxins and adjust all medications to current kidney function',
    'Maintain hemodynamic stability and individualized perfusion targets',
    'Prevent secondary insults: hypotension, sepsis progression, fluid overload'
  ]],
  ['Fluid Management in AKI', [
    'Hypovolemic AKI: early isotonic crystalloid resuscitation with reassessment',
    'Avoid both under-resuscitation and iatrogenic fluid overload',
    'Balanced crystalloids are often preferred in many critically ill settings',
    'Use dynamic markers, urine output, and bedside ultrasound when available'
  ]],
  ['Hemodynamic and Vasopressor Strategy', [
    'Persistent shock-related AKI requires timely vasopressor support',
    'Norepinephrine is typical first-line pressor in septic/distributive shock',
    'Target MAP should be individualized, especially in chronic hypertension',
    'Restoration of perfusion is central to limiting ongoing tubular ischemia'
  ]],
  ['Nephrotoxin Stewardship', [
    'Avoid or minimize aminoglycosides, amphotericin B, high-dose NSAIDs when possible',
    'Use therapeutic drug monitoring for nephrotoxic antimicrobials',
    'Hold non-essential ACEI/ARB during unstable AKI or severe hypoperfusion',
    'Review all prescriptions daily for dose, indication, and renal adjustment'
  ]],
  ['Electrolyte and Acid-Base Management', [
    'Hyperkalemia is life-threatening; monitor ECG and treat emergently when severe',
    'Address metabolic acidosis, hyperphosphatemia, hypocalcemia/hypermagnesemia as needed',
    'Use temporizing and definitive hyperkalemia therapies systematically',
    'Close laboratory surveillance is essential in dynamic AKI'
  ]],
  ['Nutrition in AKI', [
    'Provide adequate calories and avoid prolonged catabolic fasting states',
    'Protein targets should reflect illness severity and whether on RRT',
    'Restrictive strategies that worsen malnutrition should be avoided',
    'Coordinate diet with sodium, potassium, and fluid restrictions'
  ]],
  ['Indications for Renal Replacement Therapy (RRT)', [
    'Refractory hyperkalemia, severe metabolic acidosis, uremic complications',
    'Refractory fluid overload causing respiratory or hemodynamic compromise',
    'Certain intoxications and severe azotemia in selected contexts',
    'No single creatinine cutoff mandates RRT; decisions are clinical'
  ]],
  ['RRT Modalities in Critical Care AKI', [
    'Intermittent hemodialysis: efficient solute clearance for stable patients',
    'CRRT: preferred for hemodynamically unstable or cerebral edema risk',
    'SLED as hybrid option where resources/expertise support use',
    'Modality choice should be patient-centered and logistics-aware'
  ]],
  ['Timing of RRT Initiation: Current Perspective', [
    'Early versus delayed RRT remains debated in absence of urgent indications',
    'Recent trials support individualized timing rather than reflex early dialysis',
    'Watchful waiting requires close monitoring and rapid access to RRT',
    'Clinical trajectory often matters more than isolated biochemical thresholds'
  ]],
  ['Contrast-Associated AKI: Prevention', [
    'Identify high-risk patients: CKD, diabetes, hypotension, high contrast volume',
    'Use lowest feasible contrast dose and avoid repeated exposures',
    'Isotonic fluid prophylaxis remains the most consistent preventive strategy',
    'Avoid ineffective or unproven pharmacologic prophylaxis as routine care'
  ]],
  ['Sepsis-Associated AKI', [
    'Multifactorial pathogenesis: inflammation, microvascular dysfunction, hemodynamic shifts',
    'Early sepsis bundle care and source control are kidney-protective',
    'Balance resuscitation with risk of interstitial edema and venous congestion',
    'Dose antimicrobials appropriately as renal function changes over time'
  ]],
  ['Cardiorenal and Hepatorenal Contexts', [
    'AKI in heart failure reflects low perfusion and venous congestion interplay',
    'In cirrhosis, evaluate for hepatorenal syndrome after excluding other causes',
    'Therapy focuses on cause-specific hemodynamic optimization',
    'Volume status errors can worsen both renal and systemic outcomes'
  ]],
  ['Recovery Phase and Post-AKI Care', [
    'Monitor for polyuric recovery phase with electrolyte wasting',
    'Reassess drug doses frequently during renal function improvement',
    'Document AKI episode and arrange follow-up kidney function testing',
    'Post-AKI survivors need CKD risk counseling and nephrology follow-up'
  ]],
  ['AKI to CKD Transition', [
    'Incomplete tubular repair may drive chronic fibrosis and nephron loss',
    'Risk factors: severe AKI, recurrent AKI, older age, baseline CKD, diabetes',
    'Longitudinal eGFR and albuminuria surveillance is recommended',
    'Secondary prevention includes BP, glycemic, and nephrotoxin control'
  ]],
  ['Clinical Approach Algorithm (Bedside)', [
    'Step 1: Confirm AKI and stage by KDIGO using baseline and urine output',
    'Step 2: Rapidly identify reversible causes: hypoperfusion, obstruction, drugs',
    'Step 3: Use urine microscopy, indices, and ultrasound to phenotype injury',
    'Step 4: Initiate targeted treatment and monitor trajectory closely'
  ]],
  ['Case Vignette 1: Septic Shock with Oliguric AKI', [
    '65-year-old with pneumonia, hypotension, rising creatinine, urine output 0.2 mL/kg/h',
    'Priorities: sepsis bundle, perfusion optimization, nephrotoxin review, monitoring',
    'Urine sediment with granular casts suggests tubular injury pattern',
    'RRT considered if refractory hyperkalemia, acidosis, or fluid overload develops'
  ]],
  ['Case Vignette 2: Postrenal AKI', [
    '72-year-old man with anuria, suprapubic fullness, elevated creatinine',
    'Bedside bladder scan/catheterization confirms large residual volume',
    'Prompt decompression restores urine flow and improves kidney function',
    'Plan definitive evaluation for outlet obstruction etiology'
  ]],
  ['Case Vignette 3: Drug-Induced AIN', [
    'Patient on recent PPI and beta-lactam with AKI, pyuria, rash, eosinophilia',
    'Immediate discontinuation of culprit drug is essential',
    'Consider biopsy when diagnosis uncertain or recovery delayed',
    'Selected cases may benefit from corticosteroids after specialist discussion'
  ]],
  ['Key Take-Home Messages', [
    'AKI is common, dangerous, and often preventable with early recognition',
    'Structured syndrome-based evaluation outperforms isolated lab interpretation',
    'Management prioritizes cause reversal, hemodynamic support, and complication control',
    'Post-AKI follow-up is mandatory to reduce CKD progression and recurrent injury'
  ]],
  ['Suggested Reading', [
    'Harrison\'s Principles of Internal Medicine, latest edition: chapter on AKI',
    'KDIGO Clinical Practice Guideline for Acute Kidney Injury',
    'Recent RRT timing trials (AKIKI, STARRT-AKI and related analyses)',
    'Major reviews on sepsis-associated and nephrotoxin-associated AKI'
  ]]
];

slides.forEach(([title, bullets], i) => {
  const slide = pptx.addSlide();
  addTitle(slide, title, `Slide ${i + 3}`);
  addBullets(slide, bullets);
  addRef(slide, 'Primary source: Harrison\'s Principles of Internal Medicine (latest ed.); supporting nephrology/internal medicine texts.');
});

pptx.writeFile({ fileName: '/home/daytona/aki-ppt/AKI_Harrison_Residents.pptx' });