902305368.

docx
Study Guide: Kidney Disease and Urine Analysis
Part 1: Global Burden of Kidney Disease (Nature Article Review)
Source: Consensus Statement, Nature, 03/04/2024 – “Chronic Kidney Disease and
the Global Public Health Agenda: An International Consensus” by ASN, ERA, and ISN.
1.1 Importance and Objectives
 Objective: Understand the global burden of kidney diseases (KD) and the
critical need for early detection, even for non-nephrologists.
 Key Message: KD is a major driver of premature mortality, underrecognized
compared to other non-communicable diseases (NCDs) prioritized by WHO
(e.g., cardiovascular disease [CVD], stroke, respiratory disease).
 Consensus Goal: Advocate for KD inclusion on WHO’s list of major NCD
causes of premature mortality to drive global action.
1.2 Global Problem of Kidney Disease
 Mortality and Disability:
o KD is the 7th leading cause of death globally (5-11 million
deaths/year).
o Projected to rise to 5th highest cause of years of life lost (YLL) by
2040 if trends persist.
o Unlike CVD/stroke/respiratory disease, CKD mortality and burden are
increasing due to lack of detection and treatment.
o Global Burden of Disease (GBD) Study: CKD prevalence increased
by 33% from 1990–2017; third fastest-growing cause of death globally;
only NCD with rising age-adjusted mortality.
 Kidney Failure and Kidney Replacement Therapy (KRT):
o Rising numbers requiring KRT (e.g., dialysis, transplantation).
o In high-income countries (HICs), 15–20% of dialysis patients die
within 12 months of starting.
 Quality of Life and Psychosocial Impact:
o KRT (e.g., haemodialysis) is time-consuming and invasive, leading to:
 Reduced quality of life.
 Psychosocial harm (e.g., job loss, especially in countries with
limited support).
 Economic Costs:
o Direct Costs: High for governments and healthcare systems.
o Indirect Costs:
 Decreased earning potential for patients (e.g., in the USA, >75%
of new dialysis patients are unemployed due to KRT frequency—
every 2 days).
 Caregiver burden and lost productivity.
 Reduced taxation revenue for states.
o Disproportionate impact on impoverished/marginalized
communities; social determinants (poverty, poor housing, lack of
healthy food/clean water) exacerbate KD burden.

1/7
 902305368.docx
o Affects all ages, not just the elderly (e.g., children, adolescents,
pregnant/lactating women).
 Low-Income Countries (LICs) and Lower-Middle-Income Countries
(LMICs):
o Prevalence: ~850 million people worldwide have KD; most in
LICs/LMICs.
o Challenges:
 Poor healthcare infrastructure worsens outcomes.
 Lack of early detection/screening programs → large-scale
unawareness of CKD prevalence.
 9/10 individuals with CKD in resource-poor settings
unaware of their condition.
o Non-Traditional CKD Causes:
 Chronic interstitial nephritis in agricultural communities,
Mesoamerican nephropathy, Uddanam nephropathy.
 Common in the Global South (e.g., India, Sri Lanka, Africa,
Central/South America).
o Future Trends: Aging populations and population growth will increase
CKD prevalence in LICs/LMICs.
 Acute Kidney Injury (AKI) in LICs/LMICs:
o Prevalence: Affects 7–18% of hospitalized patients; 20–200 per million
annually in communities.
o Community-Acquired (75% of cases in LICs/LMICs):
 Causes: infections, toxins (animal bites, herbs, medications),
pregnancy complications.
o Underestimation: AKI’s acute nature leads to underrecognition as a
cause of death.
o Bidirectional Link: Aging reduces kidney reserve, increasing AKI risk
and progression to CKD.
 Impact on Other NCDs:
o CKD contributes to highest global age-standardized rate of
disability-adjusted life years (DALYs) (excluding
diabetes/hypertension causes).
o Systemic Disease: Kidneys regulate systemic homeostasis; CKD
worsens other NCDs (especially CVD).
o Screening Recommendation: Albuminuria screening for patients with
high cholesterol or diabetes to reduce CVD risk.
 Environmental Impact (Green Nephrology):
o Water Usage: Haemodialysis uses >500 L water/session; unsustainable
with climate change affecting water availability.
o Plastic Waste: >900,000 tonnes/year from dialysis; ~770,000 kg CO2
equivalents/facility/year in the USA; 38 million kg recyclable plastic from
peritoneal dialysis globally.
o Solutions: Early KD prevention reduces KRT need; monitoring programs
in France cut electricity/water use by 30–50%.

2/7
902305368.docx

3/7
 902305368.docx
1.3 Underrecognition of KD
 Awareness Gap: KD less recognized/feared than CVD or cancer.
 Media Underrepresentation: In US newspapers, KD 11-fold
underrepresented as a cause of death.
 Screening Deficiencies:
o Limited/no tests for kidney function in LICs/LMICs.
o Rare CKD registries globally.
 Consequence: Ineffective health system response; focus on diabetes/CVD
overlooks other KD drivers.
1.4 Aim of the Consensus Statement
 Primary Goal: Add KD to WHO’s major NCD list to:
o Enhance global campaign against KD harm, especially in emerging
economies.
o Support UN SDG 3.4 (reduce NCD premature mortality by 1/3 by 2030).
 Related SDGs Impacted:
o SDG 1 (no poverty), SDG 2 (gender equity), SDG 6 (water security), SDG
8 (work/economic growth), SDG 10 (inequalities), SDG 13 (climate
action).
 Outcomes of WHO Recognition:
o Increased global CKD awareness.
o Development of care guidelines/standards.
o Improved surveillance/monitoring.
o Coordinated international efforts for burden assessment and prevention.
o Enhanced resource allocation for new therapies.
1.5 Current Challenges and Solutions
 Challenges:
o Access to care.
o Prevention and early detection (asymptomatic early CKD; effective
interventions available).
o Novel care models.
o Awareness/education (schools, universities, media, governments).
o Social determinants (e.g., poverty).
o Funding for research/development.
o International cooperation.
o Patient community engagement.
 Solutions:
o Early detection as a cornerstone to reduce morbidity/mortality.
o Address missed opportunities to prevent kidney failure’s
health/economic/psychosocial costs.
1.6 World Kidney Day 2024
 Theme: “Kidney Health for All: Advancing Equitable Access to Care and
Optimal Medical Practice.”
 Resource: Promotional video in 204 languages on WKD website.

4/7
 902305368.docx
Part 2: Urine Analysis
Continuation from Lesson 1: Laboratory Investigations for Kidney Disease
Diagnosis
2.1 Albuminuria
 Definition: Presence of albumin in urine; key marker for kidney disease.
 Measurement Methods:
o Albumin Excretion Rate (AER): mg/24h (requires 24-hour urine
collection; compliance challenging).
o Albumin-to-Creatinine Ratio (ACR): Spot collection (e.g., morning
sample); expressed as mg/mmol or mg/g.
 Categories:
Catego AER ACR (mg/mmol or Notes
ry (mg/24h) mg/g)
A1 <30 <3 mg/mmol or <30 Normal (0 mg/24h ideal; no
mg/g prognostic difference 0–30
mg/24h).
A2 30–300 3–30 mg/mmol or 30– Microalbuminuria; red flag for
300 mg/g potential pathology.
A3 >300 >30 mg/mmol or Overt pathology; significant
>300 mg/g problem.
 Pitfalls:
o Factors Increasing Albuminuria: Exercise, fever, infection,
menstruation, heart failure, hyperglycemia.
o Factors Decreasing Albuminuria: ACE inhibitors, ARBs, low protein
diet.
o Creatinine Alterations: Muscle mass, diet, renal function affect ACR.
o Interpretation: Combine with clinical history to distinguish
physiological vs. pathological causes.
o Testing Strategy: Repeat tests to differentiate intermittent vs.
persistent albuminuria; single test insufficient for clinical decisions.
 Correlations with Other Pathologies:
o CVD: Hypertensive patients with albuminuria have worse prognosis.
o Cancer: Increased albuminuria linked to higher malignancy incidence
(reason unknown); rapid 2-year increase signals urgent intervention.

5/7
 902305368.docx
2.2 Hematuria
 Pathophysiology:
o Glomerular Origin: Damage to glomerular membrane → RBC filtration
(nephrological).
o Lower Urinary Tract (UT): Bleeding from urinary tract vasculature
distal to glomerulus (urological).
 Detection and Evaluation:
o First Line: Urine dipstick (threshold ~5–10 RBCs/µL; low sensitivity).
o Steps:
1. Differentiate: Rule out haemoglobinuria, myoglobinuria,
pigmented urine (no RBCs).
2. Confirm: Repeat test for consistency.
3. Quantify: RBC count.
4. Qualify: Morphology analysis:
 Dysmorphic RBCs: Suggest glomerular hematuria (RBCs
squeezed through damaged slit diaphragm); often with
proteinuria.
 Well-Preserved RBCs: Suggest lower UT hemorrhage.
 Associated Findings:
o Proteinuria >1 g/24h: Likely nephrogenic origin.
o Blood Casts: Glomerular origin.

6/7
 902305368.docx
2.3 Urinary Sediment
 Tools for Urine Analysis:
1. Urine Dipstick: Quick, qualitative.
2. Lab Urine Analysis: Quantitative cell counts.
3. Urinary Sediment Analysis: Light microscopy (“nephrologist’s
stethoscope”); operator-dependent, requires expertise, fresh centrifuged
urine, microscope.
 Limitations: High expertise/tools needed; preparation time-
sensitive (few hours).
 Normal Findings:
o “Silent” sediment (no remarkable elements).
o Values:
 RBCs: <5/high-power field (hpf).
 WBCs: <10/hpf.
 Epithelial cells: Low number (from lower UT).
 Pathological Elements:
1. Cells:
 RBCs: Normal (<5/hpf); dysmorphic (glomerular) vs. well-
preserved (lower UT).
 WBCs: Normal (<5/hpf).
 Neutrophils: Lower UT infections/inflammation (stones,
tumors, prostatitis, urethritis).
 Eosinophils: Drug-induced interstitial nephritis (e.g.,
penicillin).
 Lymphocytes: Early renal transplant rejection.
 Epithelial Cells:
 Tubular: Normal few; >15/10 hpf = renal disease/tubular
injury.
 Urothelial (Transitional): Few normal; increased with
infection; clumps/sheets = transitional cell carcinoma.
 Squamous: Contamination; bacteria-covered = infection.
 Neoplastic Cells: Bladder cancer.
2. Fatty Particles:
 Lipid droplets in renal epithelial cells/macrophages; “Maltese
Cross” under polarized light.
 Indicate nephrotic syndrome, diabetic nephropathy, lupus
nephritis.
3. Cylinders:
 Hyaline, granular, cellular (RBCs, WBCs, tubular cells), lipid-
containing, cerei, pigmented (bilirubin, haemoglobin, myoglobin),
mixed.
4. Crystals:

7/7
 902305368.docx
 Oxalate, triple phosphate, cystine; linked to
nephrolithiasis/metabolic disease.
5. Microorganisms: Indicate infection.

Diagnostic Table:
Condition Sediment Finding
Glomerulopathy Dysmorphic RBCs, blood casts,
proteinuria
Lower UT Well-preserved RBCs
hemorrhage
Infection Leukocytes, microorganisms
Nephrotic Fatty particles, oval fat bodies
syndrome
Nephrolithiasis Crystals (oxalate, phosphate,
cystine)
2.4 Diagnostic Integration
 Components: Signs/symptoms, family history (including systemic diseases),
lab tests (urine analysis), imaging.
 Upcoming Pathologies:
o Acute nephritic syndrome
o Nephrotic syndrome
o Isolated urine abnormality
o Acute kidney injury (AKI)
o Chronic kidney injury (CKI)
o Urinary tract infections (UTIs)
o Renal tubular defects
o Hypertension
o Urinary tract obstructions
o Urolithiasis

8/7