Chronic Kidney

Disease
What is CKD?
Chronic kidney disease is defined based on the
presence of either kidney damage or
decreased kidney function for three or more
months, irrespective of cause.
Criteria:
Duration 3 months, based on documentation
or inference
Glomerular filtration rate (GFR) <60 mL/min/1.73
m2
Kidney damage, as defined by structural abnormalities or
functional abnormalities other than decreased GFR
CHRONIC KIDNEY DISEASE
Duration 3 months, based on documentation or
inference

Duration is necessary to distinguish chronic from acute

kidney diseases.

1. Clinical evaluation can often suggest duration

2. Documentation of duration is usually not available
in epidemiologic studies
CHRONIC KIDNEY DISEASE
Glomerular filtration rate (GFR) <60 mL/min/1.73 m2

GFR is the best overall index of kidney function in health

and disease.
1. The normal GFR in young adults is approximately 125
mL/min/1.73 m2; GFR <15 mL/min/1.73 m2 is defined as
kidney failure
2. Decreased GFR can be detected by current estimating
equations for GFR based on serum creatinine
(estimated GFR) but not by serum creatinine alone
3. Decreased estimated GFR can be confirmed by
measured GFR
CHRONIC KIDNEY DISEASE
Kidney damage, as defined by structural abnormalities or functional
abnormalities other than decreased GFR

A) Pathologic abnormalities (examples). Cause is based on

underlying illness and pathology. Markers of kidney damage
may reflect pathology.

1. Glomerular diseases (diabetes, autoimmune diseases,

systemic infections, drugs, neoplasia)
2. Vascular diseases (atherosclerosis, hypertension, ischemia,
vasculitis, thrombotic microangiopathy)
3. Tubulointerstitial diseases (urinary tract infections, stones,
obstruction, drug toxicity)
4. Cystic disease (polycystic kidney disease)
CHRONIC KIDNEY DISEASE
Kidney damage, as defined by structural abnormalities or functional
abnormalities other than decreased GFR

B) History of kidney transplantation. In addition to pathologic

abnormalities observed in native kidneys, common pathologic
abnormalities include the following:

1. Chronic allograft nephropathy (non-specific findings of

tubular atrophy, interstitial fibrosis, vascular and glomerular
sclerosis)
2. Rejection
3. Drug toxicity (calcineurin inhibitors)
4. BK virus nephropathy
5. Recurrent disease (glomerular disease, oxalosis, Fabry
disease)
CHRONIC KIDNEY DISEASE
Kidney damage, as defined by structural abnormalities or functional
abnormalities other than decreased GFR

C) Albuminuria as a marker of kidney damage (increased

glomerular permeability, urine albumin-to-creatinine ratio [ACR]
>30 mg/g).*

1. The normal urine ACR in young adults is <10 mg/g. Urine ACR
categories 10-29, 30-300 and >300 mg are termed "high
normal, high, and very high" respectively. Urine ACR >2200
mg/g is accompanied by signs and symptoms of nephrotic
syndrome
2. Threshold value corresponds approximately to urine dipstick
values of trace or 1+
3. High urine ACR can be confirmed by urine albumin excretion
in a timed urine collection
CHRONIC KIDNEY DISEASE
Kidney damage, as defined by structural abnormalities or functional
abnormalities other than decreased GFR

D) Urinary sediment abnormalities as markers of kidney

damage

1. RBC casts in proliferative glomerulonephritis

2. WBC casts in pyelonephritis or interstitial nephritis
3. Oval fat bodies or fatty casts in diseases with proteinuria
4. Granular casts and renal tubular epithelial cells in many
parenchymal diseases (non-specific)
CHRONIC KIDNEY DISEASE
Kidney damage, as defined by structural abnormalities or functional
abnormalities other than decreased GFR

E) Imaging abnormalities as markers of kidney damage

(ultrasound, computed tomography and magnetic resonance
imaging with or without contrast, isotope scans, angiography).

1. Polycystic kidneys
2. Hydronephrosis due to obstruction
3. Cortical scarring due to infarcts, pyelonephritis or
vesicoureteral reflux
4. Renal masses or enlarged kidneys due to infiltrative diseases
5. Renal artery stenosis
6. Small and echogenic kidneys (common in later stages of
CKD due to many parenchymal diseases)
PATHOPHYSIOLOGY OF
CHRONIC KIDNEY DISEASE
Two broad sets of mechanisms
of damage:

1. initiating mechanisms specific to the

underlying etiology
2. a set of progressive mechanisms
- hyperfiltration and hypertrophy of the
remaining viable nephrons
PATHOPHYSIOLOGY OF
CHRONIC KIDNEY DISEASE
Increased intrarenal activity of the renin-
angiotensin axis appears to contribute
both to:
initial adaptive hyperfiltration
the subsequent maladaptive
hypertrophy and sclerosis (TGF-)
IDENTIFICATION OF RISK FACTORS AND
STAGING OF CKD
Risk factors:
1. hypertension,
2. diabetes mellitus,
3. autoimmune disease,
4. older age,
5. African ancestry,
6. a family history of renal disease,
7. a previous episode of acute kidney injury,
8. and the presence of
a. proteinuria,
b. abnormal urinary sediment, or
c. structural abnormalities of the urinary tract
Recommended Equations for Estimation of Glomerular
Filtration Rate (GFR) Using
Serum Creatinine Concentration (PCr), Age, Sex, Race, and
Body Weight
1) Equation from the Modification of Diet in Renal
Disease study (MDRD)

2) Cockcroft-Gault equation
CKD
ETIOLOGY AND EPIDEMIOLOGY
Leading Categories of Etiologies
of CKD

Diabetic glomerular disease

Glomerulonephritis
Hypertensive nephropathy
Primary glomerulopathy with
hypertension
Vascular and ischemic renal disease
Autosomal dominant polycystic kidney
disease
Other cystic and tubulointerstitial
nephropathy
TREATMENT
 TREATMENT
Any acceleration in the rate of decline should
prompt a search for superimposed acute or
subacute processes that may be reversible

1. ECFV depletion,
2. uncontrolled hypertension,
3. urinary tract infection,
4. new obstructive uropathy,
5. exposure to nephrotoxic agents
6. and reactivation or flare of the original
7. disease, such as lupus or vasculitis
 TREATMENT
SLOWING THE PROGRESSION OF CKD:
Reducing Intraglomerular Hypertension and
Proteinuria
renoprotective effect of antihypertensive medications -
proteinuria
125/75 mmHg as the target blood pressure
ACE inhibitors and ARBs
Adverse effects from these agents include cough and
angioedema with ACE inhibitors, anaphylaxis, and
hyperkalemia with either class
2nd line - diltiazem and verapamil
 TREATMENT
SLOWING PROGRESSION OF DIABETIC RENAL
DISEASE
Control of Blood Glucose
preprandial glucose be kept in the 5.07.2 mmol/L,
(90130 mg/dL)
hemoglobin A 1C should be < 7%
use and dose of oral hypoglycemic needs to be
reevaluated
Chlorpropramide
Metformin
Thiazolidinediones
 TREATMENT
SLOWING PROGRESSION OF DIABETIC RENAL
DISEASE
Control of Blood Pressure and Proteinuria

albuminuria
a strong predictor of cardiovascular events
and nephropathy
Microalbumin testing
At least ANNUALLY
 TREATMENT
SLOWING PROGRESSION OF DIABETIC RENAL
DISEASE
Protein Restriction

CKD 0.60 and 0.75 g/kg per day

at least 50% of the protein intake be of
high biologic value
Stage 5 CKD - 0.9g/kg/day
Caloric requirement 35cal/kg/day
 TREATMENT
MANAGING OTHER COMPLICATIONS OF CHRONIC
KIDNEY DISEASE
1. Medication Dose Adjustment
loading dose no dose adjustment
>70% excretion is by a nonrenal route
no adjustment
NSAIDs should be avoided
Nephrotoxic medical imaging radiocontrast
agents and gadolinium should be avoided
http://www.globalrph.com/renaldosing2.htm
 TREATMENT
MANAGING OTHER COMPLICATIONS OF CHRONIC
KIDNEY DISEASE
1. Medication Dose Adjustment
2. Preparation for Renal Replacement Therapy

symptoms and signs of impending uremia, such

as anorexia, nausea, vomiting, lassitude RX
with Protein restriction
optimal time for initiation of renal replacement
therapy have been established KDOQI
Delaying worse prognosis
 HEMODIALYSIS

ABSOLUTE INDICATIONS:
Uremic pericarditis or pleuritis
Uremic encephalopathy

Common indications:
1. Declining nutritional status
2. Persistent or difficult to treat volume overload
3. Fatigue and malaise
4. Mild cognitive impairment
5. Refractory acidosis, hyperkalemia, and
hyperphosphatemia
 TREATMENT
MANAGING OTHER COMPLICATIONS OF CHRONIC
KIDNEY DISEASE
1. Medication Dose Adjustment
2. Preparation for Renal Replacement Therapy
3. Patient Education

Kidney transplantation - offers the best potential for

complete rehabilitation
THANK YOU
Renal Potassium Handling
Renal Calcium and Phosphate
Handling
Chronic Kidney Disease
Leading Categories of Etiologies
of CKD
Chronic Kidney
Disease
NEPHROLOGY ROUNDS

Jose Socrates M. Evardone

Year Level 2
Nephrology 2
Renal Potassium Handling
Normal Lab Values