Learning Objectives

By the end of this chapter, learners will be able to:
1. Describe age-related structural and functional changes in the kidney.
2. Recognize the limitations of serum creatinine and eGFR estimates in older adults and apply practical strategies to assess renal function.
3. Identify common kidney diseases and syndromes prevalent in older adults, including AKI, CKD, obstructive uropathy, glomerular disease, and myeloma kidney.
4. Apply principles for prevention, diagnosis, and management of AKI and CKD in older adults, including individualized blood pressure and glycemic targets.
5. Optimize prescribing and deprescribing in the context of polypharmacy, frailty, and nephrotoxin stewardship.
6. Outline indications, modality selection, outcomes, and shared decision-making for renal replacement therapy (RRT) in older adults, and discuss conservative kidney management and palliative care.

26.1 Physiological Changes in the Kidney with Aging

Even in the absence of overt kidney disease, aging is associated with structural and functional changes that reduce renal reserve and increase vulnerability to kidney injury. Inter-individual variability is substantial, and comorbidities often accelerate these changes.

• Glomerular filtration rate (GFR): Mean decline of roughly 0.5–1 mL/min/1.73 m² per year from midlife, with wide variability; some older adults maintain stable GFR.
• Renal blood flow: Progressive reduction (often approximated at 5–10% per decade), reflecting vascular remodeling and endothelial dysfunction.
• Glomerulosclerosis: Increased proportion of globally sclerosed glomeruli and thickened glomerular basement membranes.
• Tubulointerstitial changes: Tubular atrophy and interstitial fibrosis; reduced nephron number; cortical thinning with modest reduction in renal mass.
• Tubular function: Impaired concentrating and diluting capacity, blunted sodium handling, decreased ammoniagenesis and acid excretion, and reduced potassium secretory reserve. Clinical implications include nocturia, susceptibility to dehydration, hyponatremia (particularly with thiazides), and hyperkalemia with RAAS blockade.
• Endocrine functions: Reduced 1-alpha hydroxylase activity and altered vitamin D metabolism; with superimposed CKD, secondary hyperparathyroidism and CKD–mineral bone disorder become more likely.
• Homeostatic reserve: Diminished capacity to respond to hemodynamic stress (e.g., sepsis, surgery) and nephrotoxins.

26.2 Challenges in Assessing Renal Function in Older Adults

Accurate estimation of kidney function is essential for diagnosis, prognosis, and drug dosing, yet is complicated by age-related changes.

• “Creatinine blind spot”:
• Reduced muscle mass and protein intake lower creatinine generation, so serum creatinine may appear “normal” despite reduced GFR.
• Avoid “rounding up” serum creatinine (e.g., to 1.0 mg/dL) in older adults—this can dangerously underestimate impairment and lead to underdosing or missed diagnoses.
• eGFR equations:
• Use contemporary, race-free equations where available. eGFR based on creatinine (eGFRcr) may overestimate GFR in sarcopenia.
• Cystatin C–based eGFR (eGFRcys) is less affected by muscle mass and can refine GFR estimates; combined creatinine–cystatin C equations (eGFRcr-cys) improve accuracy.
• At extremes of body size, diet, or in acute illness, any equation may be inaccurate; interpret in clinical context.
• Measured GFR/clearance:
• Exogenous marker clearance (e.g., iothalamate, iohexol) is the reference standard but rarely needed outside selected cases (e.g., borderline transplant evaluation, complex chemotherapy dosing).
• Timed creatinine clearance is burdensome and prone to error; it tends to overestimate true GFR due to tubular secretion.
• Drug dosing:
• Follow drug labeling and local policy. Some medications (e.g., certain DOACs) are labeled for dosing by Cockcroft–Gault creatinine clearance; others accept eGFR. When using Cockcroft–Gault, choose actual/ideal/adjusted body weight thoughtfully to avoid misclassification in frail or obese patients.
• Albuminuria and urinalysis:
• Use spot urine albumin-to-creatinine ratio (UACR) to screen and monitor proteinuria; persistent elevation indicates increased CKD progression and cardiovascular risk.
• Evaluate hematuria, pyuria, casts, and specific gravity in clinical context; interpret dipstick protein with caution in dilute or concentrated urine.
• Imaging:
• Renal ultrasound for kidney size, echogenicity, and exclusion of obstruction—especially important when post-renal AKI is suspected (e.g., BPH).
• Functional status and frailty:
• Frailty, cognition, nutrition, and falls risk materially affect decisions on targets, therapies, and modality choices.

26.3 Common Kidney Problems in Older Adults

• Acute kidney injury (AKI), often multifactorial: sepsis, hypotension, volume depletion, nephrotoxins (NSAIDs, iodinated contrast, aminoglycosides), obstruction, and cardiorenal syndromes.
• Chronic kidney disease (CKD): Diabetic and hypertensive kidney disease predominate; ischemic nephropathy and atherosclerotic renovascular disease are more frequent.
• Post-renal obstruction: Prostatic enlargement, pelvic malignancies, neurogenic bladder; high index of suspicion.
• Glomerular disease: Membranous nephropathy, ANCA-associated vasculitis, minimal change disease (often NSAID-associated), IgA nephropathy presenting later in life.
• Plasma cell dyscrasias: Cast nephropathy, light chain deposition, and amyloidosis—consider in unexplained AKI or heavy proteinuria with bland sediment.
• Recurrent or complicated urinary tract infections and catheter-associated bacteriuria; distinguish from asymptomatic bacteriuria.
• Nephrolithiasis: May present atypically; infection stones and uric acid stones more common with comorbidities.
• Electrolyte and acid–base disorders: Thiazide-associated hyponatremia, hyperkalemia with RAAS blockade, metabolic acidosis with reduced ammoniagenesis.

26.4 Acute Kidney Injury (AKI) in Older Adults

• Etiologies and risk factors:
• Hypovolemia, sepsis, heart failure, perioperative hypotension, nephrotoxins (NSAIDs, ACEi/ARB in volume depletion, diuretics, aminoglycosides), iodinated contrast, obstruction (BPH), rhabdomyolysis, and interstitial nephritis (e.g., PPIs, antibiotics).
• Clinical features:
• Oliguria may be blunted; delirium, falls, orthostasis, or nonspecific malaise are common presentations.
• Evaluation:
• Rapid assessment of volume status, vitals, medications, and urine output.
• Serum creatinine trend; electrolytes; urinalysis with microscopy; UACR if indicated.
• Bladder scan and renal ultrasound to exclude obstruction in appropriate clinical settings.
• Consider urine indices and sediment (e.g., muddy brown casts in ATN; WBCs/eosinophils in AIN; crystals).
• Management:
• Restore perfusion with cautious fluid resuscitation when hypovolemic; avoid overload in heart failure—use dynamic assessments.
• Stop nephrotoxins; adjust or hold ACEi/ARB and diuretics temporarily if contributing.
• Dose-adjust all medications to current kidney function; avoid further contrast if possible.
• Treat underlying cause (e.g., antibiotics for sepsis, relieve obstruction with catheterization and urology input).
• Monitor electrolytes and acid–base; treat hyperkalemia promptly and safely.
• Initiate RRT for standard indications (e.g., refractory hyperkalemia, acidosis, volume overload with hypoxemia, uremic complications), individualized to goals of care.
• Prevention:
• Periprocedural hydration and nephrotoxin minimization in high-risk patients.
• “Sick day” guidance during intercurrent illness (per local programs), including temporary holding of ACEi/ARB, diuretics, NSAIDs, SGLT2 inhibitors, and metformin when volume depleted or with poor intake.

26.5 Chronic Kidney Disease (CKD) in Older Adults

• Definitions and staging:
• CKD is defined by kidney damage or reduced GFR (<60 mL/min/1.73 m²) for ≥3 months. Classify by GFR (G1–G5) and albuminuria (A1–A3).
• Assessment:
• Identify etiology (history, serologies if indicated), quantify albuminuria (UACR), and evaluate for complications (anemia, mineral bone disorder, acidosis).
• Screen for obstructive uropathy when appropriate.
• Assess frailty, cognition, functional status, nutrition, and falls risk to guide targets.
• Progression risk and prognosis:
• Higher with greater albuminuria, faster eGFR decline, diabetes, uncontrolled hypertension, and recurrent AKI. Incorporate cardiovascular risk assessment.
• Management (individualize to comorbidities and tolerance):
• Blood pressure: Target SBP often <130 mmHg if tolerated; monitor for orthostatic hypotension and falls. Use home or ambulatory BP where feasible.
• RAAS blockade: ACEi/ARB for albuminuric CKD unless contraindicated; monitor creatinine and potassium after initiation or dose changes (e.g., within 1–2 weeks). Mild creatinine rise (up to ~30%) can be acceptable if stable; manage hyperkalemia risk.
• SGLT2 inhibitors: Consider in diabetic and non-diabetic CKD with albuminuria if eGFR within approved range; monitor for volume depletion and mycotic infections. Withhold during acute illness or perioperatively per local guidance.
• Glycemic control: Avoid hypoglycemia; consider agents with renal and cardiovascular benefit. Glycemic targets should be individualized, often less stringent in frail patients.
• Diuretics: Loop diuretics for volume control; thiazides may cause hyponatremia/hypokalemia—use cautiously.
• Lipids and antiplatelet therapy: Manage per cardiovascular risk and tolerance.
• Nutrition: Avoid severe protein restriction in frailty; align protein and calorie goals with nutritional status and CKD stage. Address sarcopenia with resistance exercise where feasible.
• Metabolic acidosis: Treat if serum bicarbonate persistently <22 mmol/L unless contraindicated; titrate oral alkali and monitor volume status and sodium load.
• Hyperkalemia: Dietary counseling, review of medications, potassium binders when appropriate.
• Mineral bone disorder: Monitor calcium, phosphate, PTH, and vitamin D; manage with dietary phosphate control, vitamin D repletion, and binders as indicated; avoid oversuppression of PTH.
• Anemia of CKD: Evaluate iron status; use iron therapy and consider ESAs when symptomatic or transfusion-prone, with individualized hemoglobin targets and attention to cardiovascular/thrombotic risks.
• Vaccinations: Ensure age-appropriate and CKD-specific immunizations per local guidance.
• Referral: Nephrology input for rapid progression, advanced CKD (e.g., G4–G5), refractory complications, diagnostic uncertainty, or RRT/conservative care planning.

26.6 Medication Safety and Polypharmacy

• General principles:
• Start low, go slow; reassess indication, dose, and interactions regularly.
• Deprescribe potentially inappropriate medications where risks exceed benefits, especially sedatives and anticholinergics that worsen delirium and falls.
• Align dosing with current kidney function; recheck after AKI or significant clinical change.
• High-risk or commonly implicated agents:
• NSAIDs and COX-2 inhibitors (AKI, hyperkalemia, edema).
• RAAS inhibitors (hyperkalemia, AKI in volume depletion).
• Diuretics (electrolyte disturbances, hypovolemia).
• Metformin (lactic acidosis risk with AKI or hypoxia; follow local eGFR thresholds).
• SGLT2 inhibitors (euglycemic ketoacidosis risk during acute illness; hold perioperatively).
• Aminoglycosides, vancomycin, amphotericin B, calcineurin inhibitors.
• Contrast media (iodinated and gadolinium-based; assess risk and follow local policies).
• Trimethoprim (hyperkalemia), spironolactone/eplerenone (hyperkalemia).
• Thiazides (hyponatremia), SSRIs (SIADH), PPIs (AIN, hypomagnesemia).
• Dosing methods:
• Follow drug-specific labeling for choice of eGFR vs Cockcroft–Gault CrCl when dosing; use consistent weight strategy for Cockcroft–Gault and document it.
• Monitoring:
• Check electrolytes and creatinine within 1–2 weeks of starting or adjusting ACEi/ARB, MRAs, or diuretics; sooner in high-risk patients.
• Educate on “sick day” rules to pause nephrotoxic or volume-depleting drugs during acute illness (per local guidance).

26.7 Renal Replacement Therapy (RRT) in Older Adults: Indications, Modality Choice, and Outcomes

• Indications:
• Same as younger adults (refractory hyperkalemia, acidosis, volume overload, uremic complications), within the context of goals of care, frailty, and prognosis.
• Modality selection:
• In-center hemodialysis (HD): Widely available; consider intradialytic hypotension risk, vascular access challenges, transport burden.
• Peritoneal dialysis (PD): Home-based, gentler fluid shifts, preserves residual kidney function; requires adequate manual dexterity/caregiver support and safe home environment.
• Home HD: Possible with support; benefits include flexibility and slower dialysis, but training and support needs are substantial.
• Time-limited trial: Reasonable when prognosis is uncertain; reassess functional outcomes and patient priorities.
• Access considerations:
• Weigh fistula/graft vs catheter based on life expectancy, vasculature, and urgency; avoid futile access surgery.
• Outcomes:
• Higher symptom burden, hospitalization, and mortality than younger cohorts; quality-of-life impact varies widely.
• Transplantation:
• Chronologic age alone is not an absolute contraindication; candidacy depends on comorbidities, frailty, and expected benefit.

26.8 Conservative Kidney Management and Palliative Care

• Conservative kidney management (CKM):
• Active, comprehensive care without dialysis, focusing on symptom control, optimizing medical therapy, and advance care planning.
• Appropriate for patients who are unlikely to benefit from dialysis or who decline RRT.
• Symptom management:
• Volume overload: Diuretics, dietary sodium restriction, compression therapy.
• Pruritus: Emollients, gabapentinoids with renal dosing, and other agents per local protocols.
• Restless legs: Correct iron deficiency; renally dosed dopaminergic or gabapentinoids as appropriate.
• Dyspnea, pain, nausea, sleep disturbance, depression, and anxiety: Use multimodal strategies; adjust opioids and adjuvants for kidney function.
• Communication and decision-making:
• Early discussions on prognosis, values, and treatment preferences; shared decision-making with patients and caregivers.
• Document goals of care and code status; revisit regularly, especially after hospitalizations.

26.9 Special Topics in Geriatric Nephrology

• Contrast-associated AKI prevention:
• Risk stratify; use the lowest feasible dose of low/iso-osmolar contrast; ensure adequate isotonic hydration when not contraindicated; withhold nonessential nephrotoxins. The role of N-acetylcysteine is uncertain; follow local policy.
• Obstructive uropathy:
• Consider early in AKI; assess with bladder scan/ultrasound. Relieve obstruction (e.g., Foley catheter for suspected BPH); arrange urology follow-up and alpha-blocker therapy as indicated.
• Asymptomatic bacteriuria:
• Common in older adults; do not treat unless specific indications exist (e.g., certain urologic procedures). Avoid routine urine testing without symptoms.
• Electrolyte disorders:
• Hyponatremia: Often thiazide- or SIADH-related; discontinue offending drugs, correct slowly (generally ≤8–10 mmol/L in 24 hours), and treat severe cases with hypertonic saline using careful monitoring.
• Hyperkalemia: Address contributing medications, correct acidosis, use binders when needed, and educate on dietary potassium within nutritional limits.

SUMMARY

Aging kidneys have reduced structural and functional reserve, predisposing older adults to AKI, CKD, and electrolyte disturbances. Serum creatinine can mask significant GFR decline due to sarcopenia; rely on validated eGFR equations and consider cystatin C, especially when estimates and clinical picture diverge. In AKI, promptly assess volume status, discontinue nephrotoxins, relieve obstruction, and treat underlying causes; initiate RRT for standard indications aligned with goals of care. In CKD, individualize blood pressure and glycemic targets, use RAAS blockade for albuminuria, consider SGLT2 inhibitors when appropriate, and address complications such as anemia, acidosis, and mineral bone disorder. Medication safety and deprescribing are central to care, with close monitoring after therapy changes. Decisions regarding dialysis should be individualized, incorporating frailty, function, and patient preferences; conservative kidney management with palliative care is an appropriate, active pathway for many. Early, ongoing communication and shared decision-making are paramount.

CLINICAL PEARLS

• Do not “round up” serum creatinine in older adults—this can dangerously underestimate kidney impairment.
• Consider eGFRcys or eGFRcr-cys when sarcopenia is suspected or when eGFRcr seems inconsistent with clinical status.
• Suspect obstruction early in older adults with AKI—rapid bedside bladder scan and ultrasound can be diagnostic and actionable.
• Thiazide-induced hyponatremia is common in older adults; monitor sodium shortly after initiation or dose change.
• RAAS inhibitors remain cornerstone therapy in albuminuric CKD; accept modest creatinine rise if stable, but monitor potassium closely.
• SGLT2 inhibitors may benefit eligible older adults; pause during acute illness to mitigate AKI and ketoacidosis risk.
• Avoid treating asymptomatic bacteriuria; reserve antibiotics for symptomatic infection or specific procedural indications.
• Dialysis is a treatment option, not an obligation; time-limited trials and conservative kidney management are patient-centered choices.

VISUAL MATERIALS

Suggested figures and tables for later creation:
– Diagram: Age-related structural and functional changes in the kidney (glomerulosclerosis, cortical thinning, tubular dysfunction).
– Flowchart: Evaluation of AKI in older adults (assessment, labs, ultrasound, management steps).
– Table: Comparing creatinine-, cystatin C–, and combined eGFR methods with pros/cons and use cases.
– Table: Medication classes with high nephrotoxic risk in older adults and monitoring recommendations.
– Infographic: Shared decision-making pathway for RRT vs conservative kidney management, including time-limited trial.

MULTIPLE CHOICE QUESTIONS

1) Which statement best explains why serum creatinine can be misleading in older adults?
– A. Creatinine secretion increases with age, lowering serum levels
– B. Reduced muscle mass decreases creatinine production, masking low GFR
– C. Increased dietary protein intake in older adults lowers creatinine
– D. Creatinine assays are unreliable in patients over 75 years
Answer: B
Explanation: Sarcopenia and lower creatinine generation can keep serum creatinine “normal” despite reduced GFR.

2) For a frail older adult in whom eGFRcr appears higher than clinically expected, which approach is most appropriate to refine GFR estimation?
– A. Use timed creatinine clearance in all cases
– B. Calculate eGFR using cystatin C or combined creatinine–cystatin C
– C. Round serum creatinine to 1.0 mg/dL and recalculate
– D. Assume GFR is adequate if BUN is normal
Answer: B
Explanation: Cystatin C (alone or combined with creatinine) improves accuracy in low muscle mass states; rounding creatinine is unsafe.

3) An 82-year-old with CKD G3b-A3 and diabetes is started on an ACE inhibitor. Two weeks later creatinine has risen by 22% and potassium is 5.1 mmol/L. The best next step is:
– A. Stop ACE inhibitor permanently
– B. Continue ACE inhibitor and recheck labs; provide dietary counseling for potassium
– C. Start a thiazide diuretic to lower potassium
– D. Double the ACE inhibitor dose
Answer: B
Explanation: A modest, stable creatinine rise (≤~30%) after ACEi initiation can be acceptable; monitor potassium and reassess.

4) Which is the most appropriate immediate step in an older adult with AKI and suspected bladder outlet obstruction?
– A. Start high-dose loop diuretics
– B. Order CT abdomen with contrast
– C. Perform bladder scan and insert a Foley catheter if retention is present
– D. Begin sodium bicarbonate infusion
Answer: C
Explanation: Rapid bedside assessment and relieving obstruction are priorities in post-renal AKI.

5) In older adults with albuminuric CKD, which agent class reduces CKD progression risk beyond blood pressure control?
– A. Calcium channel blockers
– B. ACE inhibitors or ARBs
– C. Alpha-blockers
– D. Nitrates
Answer: B
Explanation: RAAS blockade reduces intraglomerular pressure and proteinuria, slowing progression in albuminuric CKD.

6) Which medication strategy most reduces the risk of contrast-associated AKI in a high-risk older adult?
– A. Pre-procedure N-acetylcysteine alone
– B. Withhold nonessential nephrotoxins and provide isotonic hydration if not contraindicated
– C. Use high-osmolar contrast to reduce volume
– D. Increase diuretic dose before the procedure
Answer: B
Explanation: Nephrotoxin minimization and appropriate hydration are key preventive measures; follow local protocols.

7) Which statement about asymptomatic bacteriuria in older adults is most accurate?
– A. It should be treated to prevent CKD progression
– B. It requires antibiotics if nitrites are positive
– C. It generally should not be treated unless specific indications exist
– D. It indicates the need for chronic suppressive antibiotics
Answer: C
Explanation: Asymptomatic bacteriuria is common and typically not treated except in specific scenarios (e.g., certain urologic procedures).

8) In a newly dialyzed 79-year-old with repeated intradialytic hypotension, which modality change may reduce hemodynamic instability?
– A. Increase ultrafiltration rate
– B. Switch to peritoneal dialysis if feasible
– C. Shorten dialysis time
– D. Use higher dialysate temperature
Answer: B
Explanation: PD provides gentler fluid shifts and may improve tolerance in patients with hemodynamic instability.

9) Which is the safest correction strategy for chronic thiazide-associated hyponatremia in a symptomatic older adult?
– A. Rapid correction by 20 mmol/L in 24 hours
– B. Discontinue thiazide and correct sodium slowly, generally ≤8–10 mmol/L per 24 hours
– C. Restrict potassium intake
– D. Administer hypotonic fluids
Answer: B
Explanation: Stop the offending agent and correct gradually to prevent osmotic demyelination.

10) In an older adult with unexplained nephrotic-range proteinuria and a bland urine sediment, which diagnosis should be high on the differential?
– A. Pre-renal azotemia
– B. Membranous nephropathy
– C. Acute tubular necrosis
– D. Papillary necrosis
Answer: B
Explanation: Membranous nephropathy is a common cause of nephrotic syndrome in older adults and often presents with bland sediment.

POWERPOINT PRESENTATION (Slide Outline)

Slide 1: Title – Geriatric Nephrology: Practical Care for Older Adults
– Aging kidney physiology
– AKI/CKD care principles
– Medication safety, RRT, and CKM

Slide 2: Aging Kidneys – What Changes and Why It Matters
– Declining GFR variability
– Vascular and tubulointerstitial changes
– Clinical implications: dehydration, hyponatremia, hyperkalemia

Slide 3: Assessing Kidney Function in Older Adults
– Creatinine blind spot
– eGFRcr vs eGFRcys vs eGFRcr-cys
– When to consider measured GFR

Slide 4: Common Kidney Problems in Aging
– AKI (multifactorial)
– CKD (diabetes, hypertension)
– Obstruction, glomerular disease, myeloma kidney

Slide 5: AKI – Evaluation and Immediate Actions
– Volume status, medications, urinalysis
– Ultrasound/bladder scan for obstruction
– Stop nephrotoxins; targeted therapy

Slide 6: CKD Management – Individualized Targets
– BP, RAAS blockade, SGLT2 inhibitors
– Glycemic control; avoid hypoglycemia
– Manage anemia, acidosis, bone disease

Slide 7: Medication Safety and Deprescribing
– Start low, go slow; reassess
– High-risk drugs and monitoring
– Sick day guidance

Slide 8: RRT in Older Adults – Who, When, How
– Indications; time-limited trials
– Modality choices: HD vs PD vs home
– Access considerations and outcomes

Slide 9: Conservative Kidney Management and Palliative Care
– CKM as an active pathway
– Symptom control strategies
– Advance care planning

Slide 10: Special Topics
– Contrast risk mitigation
– Obstructive uropathy
– Asymptomatic bacteriuria

Slide 11: Case-Based Pearls
– Thiazide hyponatremia
– ACEi creatinine rise
– Hyperkalemia on RAAS blockade

Slide 12: Take-Home Messages
– Accurate assessment drives safe care
– Prevent AKI, slow CKD, align with goals
– Communicate early and often

Educational disclaimer: This chapter is for educational purposes for postgraduate clinicians. It does not replace clinical judgment, institutional policies, or specialist consultation. Therapeutic decisions should be individualized and guided by local guidelines, drug labeling, and patient-specific factors.

Visual learning: Geriatric Nephrology

Presentation resource: The Kidney Hub clinical-series PowerPoint for Chapters 22–30 accompanies these chapters for teaching use.