Practical Outpatient Algorithms — Nephrology & General Medicine

1

Outpatient Edema Workup

Bilateral pitting edema is among the most common outpatient presentations. Identify the mechanism before prescribing diuretics.

Algorithm 1 overview — Edema Workup. Begin with unilateral vs bilateral; order the targeted panel (BNP, albumin, TSH, ACR, eGFR); branch to cardiac, nephrotic, thyroid, or drug-induced cause. Anasarca or new cardiac finding = urgent referral.

Trigger

Patient presents with limb swelling or weight gain

First characterise: pitting vs non-pitting · unilateral vs bilateral · acute (<72 h) vs chronic · distribution (ankle only / below knee / anasarca)

Decision

Is the edema unilateral and acute?

Yes → DVT until proven otherwise

Apply Wells DVT score. If ≥2 points or high clinical suspicion → bilateral compression Doppler USS same day. If negative and score low → consider cellulitis, Baker's cyst ruptured, compartment syndrome, lymphedema (non-pitting, rubbery).

No → Bilateral / Chronic → Continue below

Bilateral edema almost always has a systemic cause. Proceed with mechanism-based workup.

Action

Order baseline panel for bilateral edema

Labs: Serum albumin · BNP or NT-proBNP · TSH · Urine ACR (spot) · LFTs (ALT, AST, bilirubin, PT) · eGFR/creatinine · CBC
Vitals review: BP, weight trend, O₂ saturation

Decision

What does the panel show?

BNP > 400 pg/mL

Cardiac cause likely. Request echo. Refer cardiology if new finding. Optimise loop diuretic (furosemide). Check electrolytes and renal function.

Albumin < 3.0 g/dL

Hypoalbuminaemia. Check urine protein (nephrotic if >3.5 g/day). Check LFTs for cirrhosis. Check total protein + SPEP if myeloma suspected. → Refer nephrology if nephrotic range.

TSH > 5 mIU/L

Hypothyroid edema. Classic non-pitting myxedema. Start levothyroxine; edema resolves with euthyroid state over weeks.

Decision

All labs normal — is the patient on any of these medications?

High-yield medication causes: Amlodipine / CCBs NSAIDs / mefenamic acid Pioglitazone / TZDs Pregabalin / gabapentin Minoxidil Corticosteroids Hormones / OCP

Yes → Medication-induced

Withdraw or switch offending agent. CCB-induced edema: switch to ARB + thiazide combination. Monitor for resolution over 2–4 weeks.

No → Venous insufficiency

Most common in chronic bilateral ankle edema without systemic cause. Confirm with venous duplex. Manage: compression stockings, leg elevation, sodium restriction.

Admit If

Red flags requiring urgent escalation

Anasarca with albumin <2.0 g/dL · BNP >1,000 (acute decompensated HF) · O₂ saturation <94% at rest · Creatinine acutely rising · BP >180/120 with edema · New ascites with altered sensorium (hepatic encephalopathy)

Quick Reference — edema Mechanism Map

Increased hydrostatic pressure: CHF, venous insufficiency, hypoalbuminaemia
Decreased oncotic pressure: nephrotic syndrome, cirrhosis, malnutrition
Increased capillary permeability: inflammation, allergy, infection

Lymphatic obstruction: lymphedema (non-pitting), filariasis
Sodium/water retention: CKD, medications, SIADH
Tip: Amlodipine is the most missed cause in the Philippines — always check CCB use first

2

Hyperkalemia Management

Outpatient-focused. Any K⁺ ≥ 6.0 mEq/L requires an ECG before a management decision. Type IV RTA (hyporeninaemic hypoaldosteronism) is the most common cause in CKD/DKD outpatients.

Algorithm 2 overview — Hyperkalemia Management. Classify by severity: Mild 5.0–5.5, Moderate 5.5–5.9, Severe ≥6.0 with mandatory ECG. Outpatient steps: dietary K⁺ restriction, hold offending agents, treat acidosis, consider patiromer or SZC. K⁺ ≥6.0 + ECG changes = emergency.

Trigger

Serum K⁺ above 5.0 mEq/L on routine labs

Rule out pseudohyperkalaemia first: haemolysed sample · prolonged transport (>2 h) · extreme leukocytosis or thrombocytosis (WBC >100,000 or plt >1,000,000) · fist clenching during draw. Repeat if clinical picture doesn't match.

Decision

What is the confirmed K⁺ level?

Level	Severity	Immediate Step
5.0–5.4 mEq/L	Mild	Dietary review + medication audit. Recheck in 2–4 weeks.
5.5–6.0 mEq/L	Moderate	ECG. Dietary restriction. Consider potassium binder. Reduce/hold RAASi if appropriate.
> 6.0 mEq/L	Severe	ECG immediately. If any ECG changes → ADMIT. If ECG normal and patient asymptomatic → may manage outpatient with close follow-up.

Admit If

Any ECG changes present → emergency admission

Peaked symmetrical T waves (early) · PR prolongation · Wide QRS (>120 ms) · Sine-wave pattern or VF (pre-arrest)
In-hospital: IV calcium gluconate (membrane stabilisation) → insulin + dextrose → sodium bicarbonate (if acidosis) → kayexalate/SPS enema → dialysis if refractory.

Action

Outpatient management steps (mild–moderate, no ECG changes)

1. Dietary restriction

Target <40 mEq/day (≈ 1,500 mg K⁺)
Avoid: saging (banana), abokado (avocado), kamote, mongo, coconut water
Leaching technique for vegetables (peel, cut, boil in large water, discard water)

2. Medication review

ACEi / ARB reduce dose or switch if K⁺ >5.5 with CKD
NSAIDs stop — reduce aldosterone activity
TMP-SMX stop — blocks ENaC like amiloride
K-sparing diuretics hold spironolactone if K⁺ >5.5
Loop diuretics increase dose if volume overloaded

Action

Potassium binders — when and which

Use if K⁺ persistently >5.5 mEq/L despite dietary restriction and medication optimisation, especially when RAASi continuation is clinically important (CKD progression, heart failure).

Sodium zirconium cyclosilicate (SZC / Lokelma): 10 g TID × 48 h (acute), then 5–10 g QD maintenance. Onset 1 h. Preferred in Philippines (available). Raises serum HCO₃ slightly — beneficial in CKD acidosis.
Patiromer (Veltassa): 8.4 g QD with food. Onset 7–12 h. Not interchangeable with SZC. Use away from other medications (chelates). Limited availability in PH.
Sodium polystyrene sulphonate (Kayexalate): older agent; avoid in ileus risk; PO or enema. Still widely used in PH due to cost.

Action

Treat contributing metabolic acidosis

Metabolic acidosis shifts K⁺ extracellularly (↑ K⁺ by ~0.6 mEq/L per 0.1 unit ↓ in pH). Correcting HCO₃ to ≥22 mEq/L with oral sodium bicarbonate (see Algorithm 9) reduces K⁺ by 0.3–0.6 mEq/L in CKD patients — often sufficient for mild hyperkalaemia.

Refer

Nephrology referral criteria for hyperkalaemia

K⁺ persistently >5.5 despite maximal outpatient therapy · Recurrent admissions for severe hyperkalaemia · K⁺ >5.5 with eGFR <30 (needs CKD co-management) · Suspected type IV RTA requiring diagnostic workup (renin, aldosterone levels)

Quick Reference — Hyperkalaemia Memory Aids

C-BIG-K⁺ Drop (acute treatment order): Calcium gluconate → Bicarbonate → Insulin+Glucose → Kayexalate/SZC → Dialysis
Type IV RTA: low renin + low aldosterone; K⁺ 5.0–6.0; mild NAGMA; eGFR 30–60; DKD most common cause
RAAS inhibitors: necessary for cardio-renal protection — do not stop without binder trial first

Recheck K⁺ within 1–2 weeks after any intervention
If on SZC: recheck K⁺ in 48–72 h during loading phase
Avoid raw/unprocessed bananas, kamote leaves, and coconut water in dialysis patients

3

Hyponatremia Management

Serum Na⁺ <135 mEq/L. Classify by osmolality first, then volume status. The correction rate is as important as the target — overcorrection causes osmotic demyelination syndrome (ODS).

Algorithm 3 overview — Hyponatremia Management. Step 1: serum osmolality (hypoosmolar / isoosmolar / hyperosmolar). Step 2: volume status (hypovolaemic → SIADH → hypervolaemic). Step 3: correction rate — max 8–10 mEq/L per 24h to prevent ODS. Symptomatic Na⁺ <125 = 100 mL 3% NaCl bolus.

Trigger

Serum Na⁺ <135 mEq/L found on labs

Assess symptoms: asymptomatic vs mild (nausea, headache) vs moderate (vomiting, confusion) vs severe (seizures, coma, respiratory arrest). Symptomatic hyponatraemia → hospital.

Decision

Step 1: Measure serum osmolality

Osm >290 mOsm/kg (Hypertonic)

Translocational hyponatraemia. Hyperglycaemia most common. Correct Na⁺ by +1.6 mEq/L per 100 mg/dL glucose above 100. Treat glucose — Na⁺ normalises.

Osm 280–290 mOsm/kg (Isotonic)

Pseudohyponatraemia. Extreme hyperlipidaemia or hyperproteinaemia. Measure Na⁺ on blood gas analyser (direct ISE). No treatment of Na⁺ needed.

Osm <280 mOsm/kg (Hypotonic)

True hyponatraemia. Proceed to Step 2: assess volume status.

Decision

Step 2: Assess volume status (clinical + urine studies)

Hypovolaemic (dry)

Signs: ↓ skin turgor, orthostasis, ↑ BUN/Cr ratio, dry mucosa
Urine Na <20: extra-renal loss (vomiting, diarrhoea, burns, third-spacing)
Urine Na >20: renal loss (diuretics, salt-wasting, Addison's)
Treatment: Isotonic saline 0.9%. Correct volume deficit first — Na⁺ will follow.

Euvolaemic (normal volume)

No edema, normal BP, mildly ↓ urine output
SIADH most common cause
Always rule out: hypothyroidism (TSH), cortisol deficiency (morning cortisol), medications
Medications causing SIADH: SSRIs, SNRIs, carbamazepine, TMP-SMX, PPIs, amiodarone, cyclophosphamide, oxytocin
Treatment: Fluid restriction 800–1,000 mL/day. Salt tabs. If refractory: tolvaptan (V2-receptor antagonist) — specialist-initiated only.

Hypervolaemic (edematous)

edema + ascites present
Causes: CHF, cirrhosis, nephrotic syndrome
Urine Na typically <20 (effective arterial volume depletion despite edema)
Treatment: Fluid restriction + treat underlying cause. Loop diuretic if CHF. Do not give saline.

Warning

Correction rate limits — the most important rule

Chronic hyponatraemia (>48 h or unknown duration): Maximum correction = 8–10 mEq/L per 24 hours · 18 mEq/L per 48 hours.
Faster correction → Osmotic demyelination syndrome (ODS): central pontine myelinolysis. Dysarthria, dysphagia, quadriparesis, locked-in syndrome. Irreversible.
High-risk for ODS: Alcohol use disorder · malnutrition · hypokalaemia · baseline Na⁺ <120 mEq/L · liver disease.
Acute hyponatraemia (<48 h): Can correct at 1–2 mEq/L/h initially until symptoms resolve (usually +5 mEq/L sufficient for seizures/coma).

Admit If

Symptomatic or severe hyponatraemia

Seizures, coma, obtundation, vomiting with aspiration risk → ADMIT immediately.
Emergency: 3% NaCl 150 mL IV over 20 min → repeat ×2 if no improvement → target +5 mEq/L in first hour → reassess. Stop 3% NaCl once symptomatic improvement or Na⁺ reaches 130 mEq/L.

SIADH Diagnostic Criteria (all must be met)

Serum osmolality <280 mOsm/kg · Urine osmolality >100 mOsm/kg (inappropriately concentrated)
Urine Na⁺ >40 mEq/L (renal Na wasting despite hyponatraemia) · Clinically euvolaemic
Normal thyroid function · Normal adrenal function · Not on diuretics
Common causes: CNS disease, pulmonary disease (TB, pneumonia, lung cancer), malignancy (SCLC), drugs

Na⁺ Correction Rate Estimator

Current serum Na⁺ (mEq/L)

Duration of hyponatraemia

High ODS risk factors present?

4

Resistant Hypertension

BP ≥ 140/90 mmHg on ≥ 3 maximally tolerated antihypertensive agents from different classes, including a diuretic. Pseudoresistance is far more common than true resistant hypertension — rule it out first.

Algorithm 4 overview — Resistant Hypertension. Step 1: rule out pseudoresistance (white-coat, adherence, cuff error — check 24h ABPM). Steps 2–4: optimise regimen, screen drug/lifestyle contributors, evaluate for secondary causes. Step 5: add spironolactone 25–50 mg as preferred 4th agent.

Trigger

Clinic BP ≥ 140/90 on ≥ 3 antihypertensives at adequate doses

Includes patients on ≥ 4 drugs with controlled BP (controlled resistant HTN). This accounts for ~10–20% of treated hypertensives.

Decision

Step 1: Rule out pseudoresistance — the most important step

Measurement errors

Wrong cuff size (most common) — use large cuff for arm circumference >33 cm
Talking, crossing legs, unsupported arm during measurement
Measure after 5 min rest in seated position
Check both arms — use higher reading arm

White-coat / Non-adherence

White-coat HTN: Home BP monitoring (HBPM) target <135/85 mmHg at home. ABPM gold standard (daytime avg <135/85).
Non-adherence: Pill count, pharmacy records, directly observed dosing, urine drug screen for antihypertensives (thiazide metabolite).
Suboptimal doses or inappropriate drug combinations (two ARBs, two CCBs)

Action

Step 2: Optimise current regimen before adding agents

Essential questions:
(1) Is a diuretic included? Thiazide (HCTZ/chlorthalidone) for eGFR ≥30; loop diuretic (furosemide BID) if eGFR <30 or fluid overload.
(2) Are drugs at maximum tolerated doses?
(3) Are doses timed correctly? Evening dosing of one agent improves nocturnal dipping.
(4) Single-pill combinations improve adherence — preferred where available in PH.

Action

Step 3: Identify and eliminate lifestyle and drug contributors

Lifestyle factors

Sodium intake >3 g/day (Filipino diet averages 5–6 g) — dietary recall critical
Alcohol >14 units/week raises BP significantly
OSA — very prevalent in PH; partner-reported snoring, BMI >30, Epworth ≥10 → sleep study
Weight gain, sedentary lifestyle

Pressor medications

NSAIDs (mefenamic acid, ibuprofen) — very common in PH OTC use
Decongestants (pseudoephedrine, phenylephrine)
OCP (ethinylestradiol-containing pills)
Energy drinks (caffeine + taurine)
Corticosteroids (chronic oral prednisone)
Calcineurin inhibitors (cyclosporine, tacrolimus)

Decision

Step 4: Screen for secondary hypertension

Cause	Prevalence	Clue	Screen
Primary hyperaldosteronism	Most common (~20%)	K⁺ low or low-normal; adrenal incidentaloma; severe or early-onset HTN	Aldosterone-to-renin ratio (ARR) — off interfering drugs ×2 weeks. ARR >30 with Aldo >15 → positive. Refer endocrine.
Obstructive sleep apnoea	~30–40%	Snoring, witnessed apnoeas, daytime sleepiness, obesity, thick neck	Epworth Sleepiness Scale; overnight oximetry; polysomnography. CPAP reduces SBP ~5–10 mmHg.
Renal artery stenosis	~3–5%	Flash pulmonary edema; worsening creatinine with RAASi; abdominal bruit; atherosclerotic risk; FMD (young women)	Renal Doppler USS. CTA/MRA if Doppler inconclusive. Refer vascular/nephrology.
Phaeochromocytoma	0.1–0.6%	Paroxysmal headache + sweating + palpitations triad; episodic hypertension; weight loss	24-h urine metanephrines + catecholamines (preferred) or plasma metanephrines. CT abdomen if positive.
Cushing's syndrome	Rare	Truncal obesity, proximal myopathy, purple striae, moon face, buffalo hump, easy bruising	Overnight 1 mg dexamethasone suppression test. Cortisol >1.8 μg/dL → positive. Refer endocrine.

Action

Step 5: Add 4th-line agent (true resistant HTN confirmed)

First choice: Spironolactone 25–50 mg daily (PATHWAY-2 trial: most effective 4th agent; reduces SBP ~8–9 mmHg vs placebo). Check K⁺ and eGFR at 4 weeks. Avoid if K⁺ >5.0 or eGFR <30.
If spironolactone not tolerated (gynaecomastia, hyperkalaemia):
Eplerenone 25–50 mg (more selective, less anti-androgenic) · Doxazosin 4–8 mg (α-blocker) · Bisoprolol 5–10 mg if not on BB · Moxonidine (central α-agonist, but inferior evidence).
Avoid clonidine (rebound hypertension on missed doses — dangerous in outpatient use).

Refer

When to refer to nephrology or hypertension specialist

BP uncontrolled after 4-drug regimen + lifestyle + adherence confirmed · Confirmed secondary cause (aldosteronism, RAS) · eGFR <45 with resistant HTN (likely CKD-driven; needs nephrology co-management) · Consider renal denervation evaluation at tertiary centres

4-Drug Sequence for Resistant HTN (after pseudoresistance excluded)

Step 1: RAS blocker (ACEi or ARB) + CCB (amlodipine) + Thiazide (chlorthalidone preferred over HCTZ) — maximise all doses
Step 2: Add loop diuretic if eGFR <30 or edema present (switch thiazide to furosemide BID)
Step 3: Add spironolactone 25 mg → titrate to 50 mg (PATHWAY-2 evidence)
Step 4: Add doxazosin or bisoprolol based on patient profile · Refer if still uncontrolled

5

AKI Triage — Outpatient Setting

Acute Kidney Injury (KDIGO): rise in serum creatinine ≥0.3 mg/dL within 48 h, or ×1.5 baseline within 7 days, or urine output <0.5 mL/kg/h for ≥6 h. Always compare to a prior creatinine — do not assume baseline from a single elevated value.

AKI triage outpatient algorithm — KDIGO staging table, pre/intrinsic/post-renal aetiology columns, sick-day rules ACEi/ARBs/NSAIDs/SGLT2i, admit criteria Stage 2-3 AKI oliguria rising potassium

Algorithm 5 overview — AKI Triage. KDIGO staging: Stage 1 (×1.5–1.9), Stage 2 (×2.0–2.9), Stage 3 (×3.0+). Aetiologies: pre-renal (urine Na⁺ <20), intrinsic (casts, AIN, GN), post-renal (USS). Sick-day rules: hold ACEi/ARBs, NSAIDs, SGLT2i. Admit: Stage 2–3, oliguria, rising K⁺, no reversible cause.

Trigger

Acutely elevated creatinine or oliguria on outpatient visit

First: retrieve previous creatinine. Check eHR, prior labs, old results from other facilities. A creatinine of 2.0 mg/dL may be AKI (if baseline 0.8) or chronic CKD (if stable for 2 years). This distinction drives everything.

Decision

Classify AKI severity (KDIGO staging)

Stage	Creatinine criterion	Urine output	Typical approach
Stage 1	×1.5–1.9 baseline or ↑ ≥0.3 mg/dL	<0.5 mL/kg/h × 6–12 h	Outpatient if pre-renal likely; remove offending agents; 48 h recheck
Stage 2	×2.0–2.9 baseline	<0.5 mL/kg/h × 12 h	Strong consideration for admission; close monitoring at minimum
Stage 3	×3.0 or Cr >4.0 mg/dL or initiation of KRT	<0.3 mL/kg/h × 24 h or anuria × 12 h	Admit — nephrology consult urgent

Decision

Classify aetiology: Pre-renal / Intrinsic / Post-renal

Pre-renal (most common outpatient)

History: vomiting, diarrhoea, poor oral intake, bleeding, diuretic use, heat exposure
Exam: decreased turgor, orthostasis (↑ HR or ↓ SBP ≥20 on standing), dry mucosa
Labs: BUN/Cr >20 · FENa <1% (unreliable if on diuretics — use FEUrea <35% instead) · Urine SG >1.020
Treatment: Oral/IV rehydration. Stop NSAIDs, diuretics. Hold ACEi/ARB temporarily.

Intrinsic renal

ATN: Recent contrast, aminoglycosides (amikacin), prolonged pre-renal, rhabdomyolysis (CPK elevation)
GN: Active urine sediment (dysmorphic RBCs, RBC casts), proteinuria, hematuria, hypertension, systemic symptoms (rash, arthralgias, haemoptysis)
AIN: Recent drug (NSAIDs, PPIs — especially high-dose, beta-lactam antibiotics) · rash + eosinophilia + fever (Triad present in only 10%) · FENa >1%

Post-renal (obstructive)

Classic: BPH (most common in Filipino men >60), bladder neck obstruction, pelvic malignancy, bilateral ureteric stones, neurogenic bladder
Exam: palpable bladder, suprapubic fullness, flank pain
Test: Bedside bladder USS (post-void residual >300 mL) or renal USS (hydronephrosis bilateral). Relief of obstruction often restores function rapidly.

Action

Sick-day rules — medications to hold during AKI

NSAIDs — reduce renal blood flow via prostaglandin inhibition; worst in volume depletion
ACEi / ARB — hold if volume depleted, K⁺ >5.5, or creatinine rising >25% within 2 weeks of initiation
Metformin — hold if Cr >1.5 mg/dL in women, >1.7 in men, or any AKI (lactic acidosis risk)
SGLT2 inhibitors — hold during any acute illness / hospitalisation (euglycaemic DKA risk)
Contrast agents — schedule IV contrast procedures only when renal function stable
Aminoglycosides — adjust dose per eGFR; avoid in AKI unless no alternative
Beta-blockers — continue; do not stop abruptly
Statins — continue

Admit If

Indications for hospital admission from the outpatient clinic

AKI Stage 2 or 3 · Oliguria or anuria · K⁺ >6.0 mEq/L or any ECG change · Volume overload with respiratory compromise · Creatinine rising >0.5 mg/dL in 24 h · Unknown aetiology requiring workup (GN, vasculitis) · Inability to take oral medications or maintain hydration at home · Social circumstances precluding safe outpatient monitoring

Outpatient AKI Monitoring Plan (Stage 1 Pre-renal — safe for outpatient)

Remove offending agents (NSAIDs, diuretics, RAASi temporarily)
Oral rehydration: 2–2.5 L oral fluids per day if not contraindicated by cardiac status
Recheck creatinine, electrolytes, and urine output assessment in 48–72 h
Clear return precautions: ↓ urine output, worsening edema, confusion, chest pain, BP >180/120
If not improving or worsening at 48-h recheck → escalate to admission

FeNa / FeUrea Calculator — Pre-renal vs Intrinsic AKI

Creatinine:

Urea nitrogen:

Serum Na⁺ (mEq/L)

Urine Na⁺ (mEq/L)

Serum Creatinine (mg/dL)

Urine Creatinine (mg/dL)

On diuretics? Add BUN values to calculate FeUrea (more reliable):

Serum BUN (mg/dL) (optional)

Urine BUN (mg/dL) (optional)

6

CKD Referral Thresholds

Based on KDIGO 2024 CKD guidelines. Referral is based on eGFR, albuminuria, rate of decline, and complications — not eGFR alone. Many patients with eGFR 45–60 can be safely managed in primary care with shared-care guidance.

Algorithm 6 overview — CKD Referral Thresholds (KDIGO 2024). The G×A heat-map assigns green / yellow / amber / red risk. Urgency tiers: Same week (eGFR <15, AKI-on-CKD, malignant HTN) → 4 weeks (eGFR 15–29, nephrotic) → 3 months (eGFR 30–44 + A3) → Primary care safe (eGFR ≥45 stable, A1–A2).

Trigger

CKD confirmed: eGFR <60 mL/min/1.73m² or urine ACR ≥30 mg/g on ≥2 occasions, ≥3 months apart

Confirm CKD staging using both eGFR (G1–G5) and albuminuria (A1–A3) — the G×A heatmap guides risk and referral urgency. A single creatinine is insufficient; trends over time matter most.

Urgent (<1 week)

Refer urgently — same week or emergency department

eGFR <15 mL/min/1.73m² (G5) — KRT planning required urgently
Suspected rapidly progressive GN: hematuria + proteinuria + creatinine rising over weeks (RPGN may progress to dialysis-dependence within weeks if untreated)
Hyperkalaemia >6.5 mEq/L not responding to emergency measures
Hypertensive emergency with new renal impairment
Pulmonary edema with new oliguria
Suspected hemolytic uraemic syndrome (microangiopathic hemolytic anemia + thrombocytopaenia + AKI)

Prompt (<1 month)

Refer within 4 weeks

eGFR <30 mL/min/1.73m² (G4) — KRT preparation, AVF planning, anemia management, metabolic acidosis
eGFR decline >5 mL/min/1.73m²/year (rapid progressor) or >10 mL/min in 5 years
Persistent urine ACR >300 mg/g despite optimised ACEi/ARB + BP control
Recurrent AKI episodes (>3 per year)
Difficult-to-manage HTN with CKD (suspected renovascular or secondary cause)
Inherited kidney disease: PKD, Alport syndrome, FSGS in young patient
Unexplained proteinuria >1 g/g without diabetes or HTN

Routine (<3 months)

Refer within 3 months or co-manage with nephrology guidance

eGFR 30–44 (G3b) with any of: anemia Hgb <11, metabolic acidosis HCO₃ <22, CKD-MBD (↑PTH, ↑PO₄, ↓Ca), persistent hyperkalaemia
Diabetic nephropathy G3a+ with ACR >300 despite maximal dual RAS blockade
CKD with suspected glomerular disease (hematuria + proteinuria, abnormal sediment)
CKD requiring biopsy for diagnosis (proteinuria without clear cause)

Monitor

Safe to manage in primary care — monitor per KDIGO frequency

eGFR ≥45 (G1–G3a) + ACR <30 (A1) + controlled BP + controlled diabetes → annual nephrology review may be deferred
Review frequency by G×A risk category: Low (G1–G2, A1) = annual; Moderate (G3a, A1) = annual; High (G3a A2, G3b A1) = 2×/year; Very High = 3–4×/year
Monitor: BP, eGFR, ACR, electrolytes (K⁺, HCO₃), Hgb, Ca, PO₄, PTH (if eGFR <45)

Rule of thumb: Refer when you would question your next step

eGFR <30 → always refer (G4/G5)
ACR >300 persistent → always refer
Rapidly declining eGFR → always refer
Any doubt about aetiology → refer for biopsy consideration

AVF planning: Refer vascular surgery when eGFR <25 and HD is likely trajectory — earlier creation means better maturation
Pre-dialysis education: Start when eGFR <30 — modality choice, diet, access, transplant evaluation
Transplant referral: eGFR <20 and declining — pre-emptive transplant is the best option

CKD-EPI 2021 eGFR Calculator

Creatinine units:

Serum Creatinine (mg/dL)

Age (years)

Sex assigned at birth

7

CKD anemia Workflow

anemia of CKD is a diagnosis of exclusion — always rule out iron deficiency, hemolysis, B12/folate deficiency, and GI blood loss before attributing anemia to EPO deficiency. The sequence: replete iron → reassess → consider ESA.

Algorithm 7 overview — CKD anemia Workflow. Workup first: CBC, iron studies, reticulocytes, B12/folate, LDH, stool OB. Rule out non-EPO causes. Iron repletion (IV preferred): TSAT <20% or ferritin <100. If Hgb still <10 after iron → ESA (epoetin, darbepoetin, CERA). Target Hgb 10–11.5 g/dL. ERI >10 = investigate hyporesponsiveness.

Trigger

Hgb <13 g/dL (males) or <12 g/dL (females) in a patient with CKD

CKD anemia typically normochromic normocytic. Develop earlier in CKD-DM. Nearly universal in G4–G5. Begin investigation when Hgb falls below threshold — do not wait for symptoms.

Action

Step 1: Full anemia workup — before any treatment

CBC + differential + reticulocyte count · Serum iron, TIBC, ferritin, TSAT
Vitamin B12 · Folate · LDH + haptoglobin + peripheral smear (hemolysis screen)
Faecal occult blood test (GI blood loss) · Stool H. pylori (common cause of iron deficiency in PH)
If hemolysis suspected: Direct Coombs, G6PD deficiency screen

Decision

Step 2: Is iron deficiency present?

Population	Iron deficient if	Treatment
CKD non-dialysis	Ferritin <100 ng/mL or TSAT <20%	Oral iron first-line
CKD on HD	Ferritin <200 ng/mL or TSAT <20%	IV iron preferred (poor oral absorption, inflammation)
CKD on PD	Ferritin <100 ng/mL or TSAT <20%	Oral or IV iron

Oral iron options: Ferrous sulfate 325 mg TID between meals (elemental iron 65 mg/tab) · Ferrous fumarate · Carbonyl iron (better tolerated GI-wise)
IV iron options (available in PH): Iron sucrose (Venofer) 200 mg over 30 min × 5 doses · Ferric carboxymaltose (Ferinject) 500–1000 mg single infusion (off-label in CKD; widely used)
Recheck iron stores at 3 months. A Hgb response of ≥1 g/dL in 4–6 weeks confirms iron-responsive anemia.

Decision

Step 3: After iron repletion — is Hgb still <10 g/dL?

Yes → Consider ESA

Target Hgb: 10–11.5 g/dL (KDIGO 2024 — do NOT target >13 g/dL: ↑CVD risk, stroke)
ESA options (PH): EPO-alfa (Eprex) 50–100 IU/kg SC 3×/week · Darbepoetin-alfa 0.45 mcg/kg SC Q2W · EPO-beta (NeoRecormon)
Check reticulocyte response at 2–4 weeks. Titrate dose by 25–50% if Hgb not rising.
Do not use ESA if active malignancy (promotes tumour growth), uncontrolled HTN, or pure red cell aplasia

No → Monitor

Iron-responsive anemia corrected. Recheck Hgb every 3 months. Maintain TSAT >20% and ferritin >100. Continue oral iron maintenance if oral route tolerated.

Warning

ESA hyporesponsiveness — investigate before escalating dose

Defined as: No Hgb rise ≥1 g/dL despite EPO dose >300 IU/kg/week (or darbepoetin equivalent).
Common causes: Iron deficiency (most common — recheck stores) · Active infection or inflammation (hepcidin ↑) · Hyperparathyroidism (PTH >500 suppresses erythropoiesis) · Folate/B12 deficiency · Aluminium toxicity (rare) · Dialysis inadequacy (Kt/V <1.2) · Pure red cell aplasia (anti-EPO antibodies — check if on IV EPO >3 months with sudden resistance)

Transfuse

Blood transfusion — avoid if possible, especially in transplant candidates

Avoid transfusion in pre-transplant patients — HLA sensitisation reduces transplant eligibility dramatically.
Consider transfusion if: Hgb <7 g/dL with symptoms (dyspnoea at rest, angina, altered sensorium) · Hgb <8 g/dL peri-operatively · Acute hemorrhage requiring immediate correction.
If transfusion required in transplant candidate → document, inform transplant team, request leuco-depleted filtered blood.

CKD anemia Targets — KDIGO 2024

Target Hgb: 10.0–11.5 g/dL for most CKD patients on ESA
Do NOT target Hgb >13 g/dL — TREAT (normal Hgb trial): ↑ stroke, thromboembolic events, death
Iron target: TSAT ≥20% + Ferritin >100 ng/mL (non-dialysis) or >200 (HD)
Do not give IV iron if ferritin >500 (functional iron overload risk) without reassessment
HIF-PHI (roxadustat, daprodustat): approved in some countries; monitor CVD risk; check local availability in PH

IV Iron Dose Calculator — Ganzoni Formula

hemoglobin units:

Patient weight (kg)

Current hemoglobin (g/dL)

Target hemoglobin (g/dL)

KDIGO 2024 target: 10–11.5 g/dL

Iron stores replenishment

8

Proteinuria Workup

Proteinuria on dipstick must be confirmed quantitatively and be persistent (≥2 readings ≥3 months apart) to diagnose CKD. The degree and pattern guide the diagnostic pathway.

Algorithm 8 overview — Proteinuria Workup. Quantify: spot urine ACR (A1 <30 / A2 30–300 / A3 >300 mg/g). Rule out transient causes (fever, exercise, UTI, orthostatic). Persistent = ≥2 readings over 3 months. Aetiology: DKD, hypertensive nephrosclerosis, GN, myeloma (BJP). Nephrotic threshold ACR >2200 mg/g = urgent nephrology referral.

Trigger

Positive dipstick protein (≥1+) on urinalysis

Dipstick limitations: Detects only albumin (misses light chains, tubular proteins) · False positive: concentrated urine, alkaline urine, hematuria, contamination.
Confirm with: Spot urine albumin-to-creatinine ratio (ACR) — preferred, most practical in PH outpatient setting. Alternatively, 24-hour urine protein collection (gold standard but cumbersome).

Action

Quantify proteinuria (spot urine ACR)

ACR mg/g (or mg/mmol)	Category	Clinical Significance
<30 mg/g	A1 — Normal / mildly increased	Monitor annually if CKD risk factors present
30–300 mg/g	A2 — Moderately increased	Microalbuminuria — CKD marker; maximise ACEi/ARB + SGLT2i
>300 mg/g	A3 — Severely increased	Macroalbuminuria — refer nephrology; high progression and CVD risk
>2,200 mg/g	Nephrotic range	Evaluate for nephrotic syndrome — urgent nephrology referral

Decision

Is the proteinuria transient or persistent?

Repeat ACR in 2–4 weeks. Instruct patient to avoid: vigorous exercise (within 24 h), fever, UTI, menstruation, prolonged upright posture.
Orthostatic proteinuria: Common in adolescents and young adults. Protein present only in upright urine; absent in first morning void (supine overnight). Benign; confirm with split urine collection.

Transient or orthostatic

Reassure. Repeat ACR in 6–12 months. No treatment needed. If ACR normalises and remains normal — not CKD.

Persistent (≥2 occasions)

Classify aetiology and determine CKD stage with eGFR. Proceed with workup below.

Decision

What is the likely aetiology?

Diabetic nephropathy (DN)

Diabetes + ACR 30–300 (microalbuminuria) + NO hematuria + eGFR may be normal or ↓
Typically gradual onset; bilateral kidneys normal size or enlarged
Management: ACEi or ARB (first-line) · SGLT2i (canagliflozin, empagliflozin) · BP <130/80 · HbA1c <7% · Finerenone if ACR >300 + eGFR 25–75
Refer if ACR >300 or eGFR declining despite optimised therapy

Non-diabetic proteinuria

Check: ANA, anti-dsDNA (lupus) · ANCA (vasculitis) · C3/C4 (complement-mediated) · Anti-PLA2R (MN) · SPEP/UPEP (myeloma if >40 y/o) · Hepatitis B/C serology · HIV
Active urine sediment (RBC casts, dysmorphic RBCs) → GN → urgent nephrology
Heavy proteinuria + normal urine sediment → membranous nephropathy or FSGS → refer

Nephrotic Syndrome

Nephrotic syndrome diagnosis — always refer to nephrology

Classic triad: Proteinuria >3.5 g/day + Serum albumin <3.0 g/dL + Pitting edema (± hyperlipidaemia, lipiduria).
Causes in Filipino adults: Membranous nephropathy (most common adult-onset) · FSGS · Minimal change disease (often steroid-responsive) · Amyloidosis (if myeloma, chronic infection, or FMF) · Diabetic nephropathy (if heavy).
Complications to manage while awaiting nephrology: Thromboembolism (PE risk when albumin <2.0 — consider anticoagulation) · Infection risk (encapsulated organisms — vaccinate) · Hyperlipidaemia (statin).

Proteinuria Workup Summary — Outpatient Approach

Confirm: Repeat spot ACR × 2 readings, ≥3 months apart
Quantify: ACR (spot) or 24-h urine protein (if ACR inconclusive)
Characterise: Urine microscopy (casts, dysmorphic RBCs?)
Baseline: eGFR, electrolytes, albumin, LFTs, CBC, BP

Diabetic: ACEi/ARB + SGLT2i + BP control → refer if ACR >300 or declining
Non-diabetic + hematuria + casts → GN → urgent nephrology
Nephrotic range → always refer → biopsy usually required
ACR 30–300 stable + diabetes/HTN controlled → manage in primary care

9

Metabolic Acidosis Correction

Step-wise approach: confirm the primary disorder, calculate the anion gap (with albumin correction), classify, then treat the cause. CKD metabolic acidosis (Type IV RTA and uraemic acidosis) are the most common outpatient presentations.

Metabolic acidosis workup algorithm — confirm pH HCO3, anion gap calculation with albumin correction, high AG MUDPILES mnemonic, normal AG HARDDUP RTA types I II IV, CKD treatment oral sodium bicarbonate, pH below 7.2 referral

Algorithm 9 overview — Metabolic Acidosis. Confirm: pH <7.35, HCO₃ <22. Calculate AG (Na − Cl − HCO₃; correct for albumin). High AG (MUDPILES): uremia, DKA, lactic acidosis, toxins. Normal AG (HARDDUP): hyperchloraemic — RTA types I/II/IV, diarrhoea. CKD treatment: oral NaHCO₃, target HCO₃ >22. Refer if pH <7.2.

Trigger

ABG or venous blood gas showing pH <7.35 with HCO₃ <22 mEq/L

Step 1: Confirm primary disorder and assess compensation.
Winter's formula (expected pCO₂ for pure metabolic acidosis):

Expected pCO₂ = (1.5 × HCO₃) + 8 ± 2 If measured pCO₂ < expected → concurrent respiratory alkalosis If measured pCO₂ > expected → concurrent respiratory acidosis (e.g., COPD)

Action

Step 2: Calculate anion gap (AG) and correct for albumin

AG = Na⁺ − (Cl⁻ + HCO₃⁻) Normal: 8–12 mEq/L Albumin-corrected AG = measured AG + [2.5 × (4.0 − albumin g/dL)] ↑ by 2.5 mEq/L for each 1 g/dL drop in albumin below 4.0 Delta-delta ratio (if high AG present): δδ = (AG − 12) / (24 − HCO₃) <0.4 → pure NAGMA (no AG component) 0.4–2 → pure HAGMA >2 → HAGMA + concurrent metabolic alkalosis

Decision

Step 3: Classify by anion gap

High AG metabolic acidosis (HAGMA)

MUDPILES mnemonic:

Methanol poisoning
Uraemia (CKD G4–G5)
DKA / alcoholic / starvation ketoacidosis
Propylene glycol (IV medications)
Isoniazid / Iron toxicity
Lactic acidosis (Type A: hypoperfusion; Type B: metformin, liver disease)
Ethylene glycol (antifreeze)
Salicylate toxicity

Calculate osmolar gap if toxic alcohol suspected: OG = measured Osm − calculated Osm. OG >10 → toxic alcohol.

Normal AG (NAGMA / hyperchloraemic)

Calculate urine anion gap (UAG):

UAG = UNa + UK − UCl

Negative UAG (−): Appropriate NH₄⁺ excretion. Extra-renal cause: diarrhoea (most common in PH), ileostomy, fistula. → Treat with oral NaHCO₃ or K-citrate.
Positive UAG (+): Impaired NH₄⁺ excretion → Renal tubular acidosis (RTA).

Action

RTA classification (positive UAG = impaired renal acidification)

Type	Urine pH	K⁺	HCO₃	Cause	Action
Type I (Distal)	>5.5 (can't acidify)	Low	Variable (often <15)	Sjögren's, autoimmune, amphotericin, nephrocalcinosis/stones	NaHCO₃ or K-citrate. Refer nephrology.
Type II (Proximal)	<5.5 (can acidify, but leaks HCO₃)	Low	<15 mEq/L	Fanconi syndrome, myeloma, tenofovir, heavy metals	High-dose NaHCO₃ (often 10+ mEq/kg/day). Refer nephrology.
Type IV (Hypoaldosteronism)	<5.5	High	Mild reduction (18–22)	Most common in CKD/DKD, ACEi/ARB use — hyporeninaemic hypoaldosteronism	Treat hyperkalaemia (Algorithm 2). Fludrocortisone if confirmed Addison's. Often improves with NaHCO₃ + K⁺ management.

Action

CKD metabolic acidosis — outpatient treatment (most common scenario)

Target: serum HCO₃ ≥22 mEq/L (KDIGO 2024 — slows CKD progression, preserves muscle mass, improves bone health, reduces hospitalisation).

Sodium bicarbonate (NaHCO₃):
Starting dose: 0.5–1.0 mEq/kg/day divided into 2–3 doses with meals
Tablet: NaHCO₃ 650 mg = 7.7 mEq HCO₃ (available in PH pharmacies)
Powder: Baking soda (sodium bicarbonate) 1 level teaspoon = 48 mEq — practical and inexpensive for PH patients
Titrate every 4 weeks until HCO₃ reaches 22–26 mEq/L

Caution with sodium load: Each gram NaHCO₃ = 12 mEq Na⁺ — monitor BP and edema. If fluid overload is a concern, consider potassium citrate (if K⁺ is normal or low) as a sodium-free alternative.

Benefits beyond acidosis correction: Improved muscle protein retention · Reduced phosphate release from bone · Better response to EPO · Reduced hyperkalaemia (see Algorithm 2)

Refer

When to refer metabolic acidosis to nephrology or toxicology

Severe acidaemia: pH <7.20 or HCO₃ <10 → hospital (may need IV NaHCO₃ or haemodialysis) · Lactic acidosis type A (sepsis, shock) → ICU · Toxic alcohol ingestion (methanol, ethylene glycol) → emergency department + toxicology · Type I or II RTA with nephrocalcinosis/stones or Fanconi syndrome → nephrology · CKD acidosis not responding to oral NaHCO₃ at 1 mEq/kg/day → nephrology co-management

Quick Reference — Metabolic Acidosis Formulas

Anion gap: Na − (Cl + HCO₃) · Normal 8–12 mEq/L
Albumin correction: AG + 2.5 × (4 − Alb)
Winter's formula: pCO₂ = (1.5 × HCO₃) + 8 ± 2
Delta-delta: (AG−12) / (24−HCO₃)

Urine AG: UNa + UK − UCl · Negative = GI loss · Positive = RTA
NaHCO₃ 650 mg tab = 7.7 mEq HCO₃
Baking soda 1 tsp = ~48 mEq NaHCO₃ (practical for home use)
Type IV RTA = most common CKD acidosis; hyperkalemia + mild NAGMA in DKD

Anion Gap, Delta-Delta & Bicarbonate Deficit Calculator

Albumin units:

Serum Na⁺ (mEq/L)

Serum Cl⁻ (mEq/L)

Serum HCO₃⁻ (mEq/L)

Serum Albumin (g/dL)

For corrected AG. Normal = 4.0 g/dL.

Measured pCO₂ (mmHg) (optional)

Weight (kg) (for HCO₃ deficit)

Practical Outpatient Algorithms
9 rapid decision pathways for nephrology & general medicine

Outpatient Edema Workup

Quick Reference — edema Mechanism Map

Hyperkalemia Management

Quick Reference — Hyperkalaemia Memory Aids

Hyponatremia Management

SIADH Diagnostic Criteria (all must be met)

Resistant Hypertension

4-Drug Sequence for Resistant HTN (after pseudoresistance excluded)

AKI Triage — Outpatient Setting

Outpatient AKI Monitoring Plan (Stage 1 Pre-renal — safe for outpatient)

CKD Referral Thresholds

Rule of thumb: Refer when you would question your next step

CKD anemia Workflow

CKD anemia Targets — KDIGO 2024

Proteinuria Workup

Proteinuria Workup Summary — Outpatient Approach

Metabolic Acidosis Correction

Quick Reference — Metabolic Acidosis Formulas

W. G. M. Rivero, MD, FPCP, DPSN

Practical Outpatient Algorithms9 rapid decision pathways for nephrology & general medicine

Outpatient Edema Workup

Quick Reference — edema Mechanism Map

Hyperkalemia Management

Quick Reference — Hyperkalaemia Memory Aids

Hyponatremia Management

SIADH Diagnostic Criteria (all must be met)

Resistant Hypertension

4-Drug Sequence for Resistant HTN (after pseudoresistance excluded)

AKI Triage — Outpatient Setting

Outpatient AKI Monitoring Plan (Stage 1 Pre-renal — safe for outpatient)

CKD Referral Thresholds

Rule of thumb: Refer when you would question your next step

CKD anemia Workflow

CKD anemia Targets — KDIGO 2024

Proteinuria Workup

Proteinuria Workup Summary — Outpatient Approach

Metabolic Acidosis Correction

Quick Reference — Metabolic Acidosis Formulas

W. G. M. Rivero, MD, FPCP, DPSN

Practical Outpatient Algorithms
9 rapid decision pathways for nephrology & general medicine