Renal Failure

SMF Urologi
FK-Unpar / RSUD dr. Doris Sylvanus
 Renal Failure
Acute Renal Failure
A sudden deterioration of renal function
resulting in the inability of the kidney to
regulate fluid and solute balance
 There is a rapid decline in glomerular
filtration rate that is accompanied by an
increase in serum creatinin level of at least
0,5 to 1,0 mg/dl
 Pre renal azotemia

Post Renal
ARF Azotemia or
obstructive uropathy

Acute intrinsic
Renal Failure
(Renal
Paranchyma)
 The Spectrum of Renal Disease
Urology Nephrology

Asymptomatic urinary abnormality

(usually hematuria/proteinuria

Nephritis Nephrotic
stones
Tumor Acute
syndrome

Renal Failure
Tubular
Obstruction Infection Hypertension
disorders

Recovery
possible

Recovery to
normal no
Chronic
longer
Renal Failure
possible

End Stage
Renal Failure
The Spectrum of Renal Disease
Many cause of ARF are potentially
reversible, and delay is of long duration (6
months or longer) Recovery is unlikely
Etiology, Pathogenesis,
and Management of
Renal Failure
Prerenal Causes of Acute Renal Failure
Volume Depletion
Surgical : hemorrhage, shock
Gastrointestinal losses : vomiting, diarrhea, fistulas
Renal : overdiuresis, salt-wasting disordes
Cardiac Causes : Primary Decrease in Cardiac Output
Acute disorders : myocardial infarction, arrhyththmias, malignant
hypertension, tamponade, endocarditis
Chronic disorders : valvulae diseases, chronic cardiomyopathy (ischemic
heart disease, hypertensive heart disease)
Redistribution of Extracellular Fluid
Hypoalbuminemic states : nephrotic syndrome, advanced liver disease,
malnutrition
Physical causes : peritonitis, burns, crush injury
Peripheral vasodilatation : sepsis, antihypertensive agents
Renal artery stenosis (bilateral)
 Differential Diagnosis of Rapidly Progressive
Glomerulonephritis
Multisystem Diseases
Systemic lupus erythematosus
Goodpastures disease
Henoch-Schnlein purpura
Necrotizing vasculitis (including Wegeners granulomatosis)
Cryoglobulinemia (hepatitis B or C related)
Neoplasia (colon, lung)
Relapsing polychondritis
Behcets disease

Superimposed on Primary Glomerular Disease

Membranoproliferative glomerulonephritis (type I, II)
Membranous glomerulonephritis
IgA nephropathy
Infectious Diseases
Post-streptococcal glomerulonephritis
Infectious endocarditis
Visceral sepsis
Hepatitis B or hepatitis C infection

Drug and Toxic Agents

Allopurinol
D-Penicillamine
Hydralazine
Rifampin

Idiopathic
Type I : antiglomerular basement membrane antibody disease
Type II : immune complex-mediated disease
Type III : pauci-immune (antineutrophil cytoplasmic autoantibody positive)
Drugs That Cause Acute Interstitial Nephritis
Nonsteroidal anti-inflammatory agents (particularly
fenoprofen)
Penicillins and cephalosporins
Rifampin
Sulfonamides (furosemide, bumetanide, thiazide-type diuretics
and trimethoprim-su;famethoxazole)
Climetidine
Allopurinol
Ciprofloxacin and perjaps other quinolones
5-Aminosalicylates
Causes of Exogenous Toxic Acute Renal Failure

Antibiotics
Aminoglycosides
Cephalosporins
Sulfonamide, co-trimoxazole
Tetracyclines
Amphotericin B
Polymyxin, colistin
Bacitracin
Pentamidine
Vancomycin
Acyclovir
Foscarnet
Anesthetic Agents
Methoxyflurane
Enflurane

Contrast Media
Diatrizoate
Iothalamate
Bunamiodyl
Iopanoic acid

Antiulcer Regimens
Climetidine
Excess of milk-alkali
Diuretics
Mercurials
Ticrynafen

Chemotherapeutic and
Immunosuppressive Agents
Cisplatin
Carboplatin
Ifosmide
Methotreaxate
Nitrosourea
Plicamycin
Cyclosporine
Tacrolimus
D-Penicillamine
Recombinant interleukin-2
Interferon
Analgesics
Nonsteroidal anti-inflammatory drugs

HIV Protease Inhibitors

Indinavir
Ritonavir

Organic Solvents
Glycols (ethylene glycol, diethylene glycol)
Halogenated hydrocarbons (CCL, tetrachloroethylene
and trichloroethylene)
Aromatic hydrocarbons (Toluene)
Aliphatic-aromatic hydrocarbons
5-Azacytidine (petrolatum [Vaseline], kerosene, turpentine,
paraphenylene diamine)
Heavy Metals and Poisons
Insecticides (chlordane)
Herbicides (paraquat, diquat)
Rodenticide (elemental phosphorus)
Mushroom
Snake bites*
Stings*
Bacterial toxins*

Chemicals
Aniline
Hexol
Cresol
Chlorates
Potassium bromate

*Direct toxicity or indirect systemic effects (shock, intravascular hemolysis, or coagulation)

Recreational Drugs
Heroin
Amphetamine

Miscellaneous
Dextrans
EDTA0
Radiation
Silicone
-Aminocaproic acid*
Angiotensin-converting enzyme inhibitors
*Direct toxicity or indirect systemic effects (shock, intravascular hemolysis, or coagulation)
Slow onset of renal failure unless associated with rhabdomyolysis.
Acute Renal Failure Related to Endogenous
Nephrotoxic Products
Pigment Nephropathy
Myoglobin
Hemoglobin*
Metheglobin*

Intrarenal Crystal Deposition

Uric acid
Calcium
Oxalate

Tumor-Specific Syndromes
Tumor lysis syndrome
Plasma cell dyscrasias (e.g. myeloma kidney)

*Questionable direct nephrotoxic effect.

Urine Sediment in Acute Renal Failure
Sediment Findings Diagnosis

Normal Prerenal/obstruction
Red blood cell casts, red Acute
blood cell glomerulonephritis/vasculitis
Eosinophils Acute interstitial nephritis
Pigmented granular casts Acute tubular necrosis
Patterns of Urinary Indices in Acute Renal Failure
Prerenal/Acute Acute Tubular
Glorulonephritis Necrosis/Obstruction

Urinary [Na+] mEq/L <20 >40

Urine : plasma creatinine >30 <20
Renal failure index <1 >1
FENa <1 >1
Urinary osmolality >500 <400
 Complication of Acute Renal Failure

Fluid Overload
Hypertension
Edema
Acute pulmonary edema

Electrolyte Disturbances
Hyponatremia
Hyperkalemia
Hypermagnesemia
Hyperphosphatemia
Hypocalcemia
Hyperuricemia (post rhabdomyolysis)
Hyperuricemia
Metabolic acidosis
Uremic Signs and Symptoms

Gastrointestinal
Nausea
Vomiting
Upper gastrointestinal bleeding
Neurologic
Mental status changes
Encephalopathy
Coma
Seizures
Peripheral neuropathy
Cardiac
Pericarditis
Uremic cardiomyopathy
Pulmonary
Pleuritis
Uremic cardiomyopathy
Hematologic
Bleeding
Anemia
Immunologic
Impaired granulocyte function
Impaired lymphocyte function
Conservative Medical Management of Acute Tubular Necrosis

Fluid Balance
Carefully monitor intake/output and weights
Restrict fluids

Electrolytes and Acid-Base Balance

Prevent and treat hyperkalemia
Avoid hyponatremia
Keep serum bicarbonate >15 mEq/L
Minimize hyperphosphatemia
Treat hypocalcemia only if symptomatic or if intravenous bicarbonate is required

Uremia and Nutrition

Administer protein (1.0-1.8 g/kg/day) and maintain caloric intake; considers forms of
nutritional support
Keep carbohydrate intake at least 100 f/day to minimize ketosis and endogenous protein
catabolism

Drugs
Review all medications
Stop magnesium-containing medications
Adjust dosage for renal failure; readjust with improvement of glomerular filtration rate
 KEY POINTS : ACUTE RENAL FAILURE

Creatinine as an assessment of renal function needs to be

interpreted in the context of clinical events that are
occurring in the patient.
Acute renal failure is categorized based on
pathophysiology as prerenal, postrenal, or intrinsic renal.
The etiology and the pathogenesis determine
management.
Prerenal azotemia is transient renal hypoperfusion and
responds well to isotonic fluid replacement.
In considering posttrenal causes of ARF, do not forgrt for
therapeutic intervention.
Conservative management predominates for ATN. This
entails dialysis support as needed with prevention of
complications.
 Review of the data regarding pharmacologic intervention
for established ATN supports a trial of isotonic fluid
repletion. Judicious use of intravenous loop diuretics may
increase urine output, but the ability of these agents to have
an impact on improved patient survival in ARF is still not
proven. Similarly, the clinical data onrenal-dose dopamine
are scant and do not support its widespread use in
established ATN.
Recommendations for the azotemic patients who require
radiocontrast procedures warrant a protocol of intravenous
hydration and the use of nonionic contrast material in the
lowest dose possible. Treatment with N-acetylcysteine for
48 hours before the procedure and/or special hydration with
prestudy sodium bicarbonate are deserving of further study.
Clinical Action Plan for Chronic Kidney Disease by Glomerular
Filtration Rate Levels
Stage Description
At increased risk
Kidney damage with normal or
increased GFR
Kidney damage with mild
decrease in GFR
Moderate decrease in GFR
Severe decrease in GFR
Kidney failure
GFR (mL/min/1.73 m2) Action
90 (with CKD risk factors) Screening, CKD reduction
90 Diagnosis and treatment,
treatment of comorbid
conditions, slowing
progression, cardiovascular
risk reduction.
60 to 89
Estimating progression
Evaluating and treating
30 to 59 complications
15 to 29 Evaluating and treating
complications
<15 (or dialysis) Replacement (if uremia
present)
Incidence of Reported End-Stage Renal Disease by
Detailed Primary Renal Diagnosis, 1998-2002
Diagnosis %

Diabetes mellitus 49.3*

Hypertensive/large vessel disease 26.9
Glomerulonephritis 8.9
Secondary glomerulonephritis/vasculitis 2.2
Interstitial nephritis/pyelonephritis 4.2
Cause uncertain 3.9
Miscellaneous 4.1
Cystic hereditary/congenital disease 3.2
Neoplasms/tumor 2.0
Missing 1.5

*Type 1 juvennile, 4.7%; type 2 adult onset or unspecified, 44.6%

Sickle cell disease; AIDS nephropathy; traumatic, surgical loss of kidney; hepatorenal syndrome;
tubular necrosis without recovery, postpartum renal failure.
Prevalence of Individuals at Increased Risk for Chronic Kidney
Disease
Prevalence
Risk Factor Estimated % Estimated No.

Diabetes mellitus Diagnosed: 5.1% of adults age 10.2 million

20
Undiagnosed: 2.7% of adults
age 20
Hypertension 24.0% of adults age 18 43.1 million
Systemic lupus erythematosus ~0.05% definite or suspected ~239,000
Functioning kidney graft ~0.03% 88,311 as of 12/31/1998
African American 12.3% 34.7 million
Hispanic or Latino (of any race) 12.5% 35.3 million
American Indian and Alaska Native 0.9 2.5 million
Age 60 to 70 7.3% 20.3 million
Age 70 92.0% 25.5 million
Acute kidney failure ~0.14% ~363,000 nonfederal hospital
stays in 1997
Daily use of nonsteroidal anti- ~5.2 % with rheumatoid arthritis ~13 million assumed daily
inflammatory drug or osteoarthritis (assumed daily use
use)- ~30% yearly use
~75 million yearly use
Causes of Progressive Chronic Kidney Disease

Tubulointerstitial
Hematopoietic: sickle cell disease, lymphoproliferative, dysproteinemia,
neoplastic.
Urologic: ureteral obstructions, reflux, prune-belly syndrome, prostatic
hypertrophy
Vascular: radiation, hypertension, atheroemboli
Metabolic: cystinosis, oxalosis, uric acid nephropathy, hypercalcemia
Immunologic: renal allograft rejection, Sjgrens syndrome
Toxic: analgesic, nonsteroidal anti-inflammatory drugs, chemotherapy
Immunosuppression: tacrolimus, cyclosporine
Heavy metals: lead, lithium

Hereditary
Sickle cell disease
Cystic disease: autosomal dominant polycystic kidney disease,
medullary cystictic disease
Alports syndrome
Karyomegalic interstitial nephritis
Primary Renal Disease
Glomerular: idiopathic glomerulonephritis
Minimal change disease
Focal segmental glomerulosclerosis
Membranous glomerulonephritis
IgA nephropathy

Systemic Diseases
Diabetes mellitus
Infection-related glomerulonephritis
Systemic lupus erythematosus, Henoch-Schnlein purpura, systemic sclerosis
Dysproteinemias/amyloid
Thrombotic microangiopathies
Vasculitis: crescentic glomerulonephritis, acute diffuse
glomerulonephritis, antineutrophil cytoplasmic antibody
glomerulonephritis (microscopic polyangiitis), Wegeners
granulomatosis, Churg-Strauss syndrome, Goodpastures syndrome,
granular cell arteritis
Factors Associated with Acute Deteriorations in Chronic
Kidney Disease

Nephrotoxic
Pharmacologist agents
Aminoglycoside antibiotics
Nonsteroidal anti-inflammatory drugs
Cyclooxygenase-2 inhibitors
Chemotherapeutics agents
Anti-rejection agents (cyclosporine, tacrolimus)
Anesthetic agents

Autoregulatory Dysfunction
Angiotensin-converting enzyme inhibitors
Angiotensin receptor blocker
Anatomic/Structural
Autosomal dominant polycystic kidney disease and angiotensin-converting
enzyme inhibitors
Obstruction
Progressive renal artery stenosis
Renal vein thrombosis
Nephrolithiasis

Hemodynamic/Perfusion Disorders
Congestive heart failure
Peroperative hypotension
Volume depletion
Gastrointestinal: bleeding, diarrhea, vomiting
Excessive diuresis
Sepsis with vasodilation

Parenchymal Injury
Acute myocardial infarction
Valvular dysfunction
Superimposed new glomerulomephritis
Interstitial
Hypercalcemia
Hyperuricosuria
Atheroemboli

Drug-Induced
Penicillin analogs
Cephalosporins
Sulfonamides
Rifampin
Diuretics
Thiazide
Furosemide

Miscellaneous
Phenytain
Allopurinol
Cimetidine
Comprehensive Renoprotection Strategy
Focus Area
Blood pressure cntrol
Reduction in proteinuria
Glycemic control
Dietary protein restriction
Lipid lowering
Anemia management
Lifestyle modifications
Calcium X phosphorus product
Goal Treatment
< 130/80 if proteinuria <1 g/day Angiotensin-converting enzyme inhibitor
< 125/75 if proteinuria >1 g/day Angiotensin receptor blocker
Salt restriction
Diuresis
< 0.5 g/day Angiotensin-converting enzyme inhibitor
Angiotensin receptor blocker
? Aldosterone blockade
HbA1C < 7% Oral hypoglycemic agents
Diet
Insulin
0.6 to 0.8 g/kg/d Dietary consult
Low-density lipoprotein level 70 mg/dL Statin
Triglyceride-lowering agent
Hemoglobin > 12 g/dL Erythropoietin
Iron
Ideal body weight Weight loss program (dietary counseling,
Smoking cessation surgery)
Exercise three times per week Antidepressants
Depression modification
< 4.5 mmol/L Vitamin D supplementation
< 55 mg/dL Use of dietary phosphorus restriction
Phosphorus < 5.5 mg/dL (1.78 mmol) Phosphate binders
(CKD stage 4)
30 70 pg/mL (CKD stage 3)
25(OH) vitamin D > 30 ng/mL
Causes of End-Stage Renal Disease in Worldwide
Renal Registries
ISRDS CORR ANZDATA JSDT
Incidence
Diabetes 49.3 28.2 18.6 33.8
Hypertension 26.9 9.9 9.7 6.5
Glomerulonephritis 8.9 16.1 34.5 38.2

Point Prevalence
Diabetes 35.7 23.0 29.6 21.7
Hypertension 23.7 9.3 12.2 3.9
glomerulonephritis 15.6 20.3 22.0 53.5
 Expected Remaining Liftimes (Year) of the General US Population, and of Prevalent Dialysis and transplant
Patients, by Race and Gender from the 2004 USRDS Annual Data Report
General U.S. Population, 2001
All Races White Black
Age All M F All M F All M F
0 77.2 74.4 79.8 77.7 75.0 80.2 72.2 68.6 75.5
1 76.7 74.0 79.3 77.1 74.5 79.6 72.2 68.6 75.4
5 72.8 70.1 75.4 73.2 70.6 75.7 68.3 64.8 71.5
10 67.9 65.2 70.4 68.3 65.6 70.8 63.4 59.8 66.6
15 62.9 60.2 65.5 63.3 60.7 65.8 58.5 54.9 61.7
20 58.1 55.5 60.6 58.5 56.0 60.9 53.7 50.3 56.8
25 53.4 50.9 55.7 53.8 51.3 56.1 49.1 45.8 52.0
30 48.6 46.2 50.9 49.0 46.6 51.2 44.5 41.4 47.2
35 43.9 41.5 46.0 44.2 41.9 46.3 39.5 36.9 42.5
40 39.2 37.0 41.3 39.5 37.3 41.6 35.5 32.5 38.0
45 34.7 32.5 36.6 34.9 32.8 36.9 31.2 28.4 33.6
50 30.3 28.2 32.1 30.5 28.4 32.3 27.1 24.4 29.3
55 26.0 24.0 27.7 26.1 24.2 27.8 23.3 20.8 25.3
60 21.9 20.1 23.4 22.0 20.2 23.5 19.7 1705. 21.5
65 18.1 16.4 19.4 18.2 16.5 19.5 16.4 14.4 17.9
70 14.6 13.1 15.7 14.6 13.2 15.7 13.5 11.7 14.7
75 11.5 10.2 12.4 11.5 10.2 12.3 10.8 9.3 11.7
80 8.8 7.7 9.4 8.7 7.7 9.3 8.6 7.3 9.2
85 6.5 5.7 6.9 6.4 5.6 6.7 6.7 5.7 7.0

90 4.8 4.2 5.0 4.6 4.1 4.8 5.1 4.5 5.3

95 3.6 3.2 3.7 3.4 3.0 3.4 3.9 3.6 4.0
100 2.7 2.5 2.8 2.4 2.3 2.5 3.0 2.9 3.0
Expected Remaining Liftimes (Year) of the General US Population, and of Prevalent Dialysis and transplant
Patients, by Race and Gender from the 2004 USRDS Annual Data Report

ESDR: Dialysis 2002

All Races White Black Native American Asian
Age All M F All M F All M F All M F All M F
0-14 20.1 21.2 18.9 20.1 21.0 19.1 19.0 20.5 17.5 22.9 23.4 22.5 32.2 32.8 31.5
15-19 17.2 18.1 16.1 16.6 17.4 15.8 17.1 18.5 15.8 18.4 18.9 17.9 25.0 25.5 24.5
20-24 14.6 15.5 13.6 14.0 14.6 13.2 14.8 16.1 13.4 15.3 15.9 14.9 21.8 22.2 21.3
25-29 12.5 13.2 11.7 11.8 12.3 11.1 13.0 14.0 11.9 12.8 13.1 12.6 18.9 19.2 18.5
30-34 10.8 11.3 10.2 9.9 10.2 9.5 11.5 12.3 10.6 11.1 11.1 11.1 16.2 16.4 16.0
35-39 9.3 9.6 8.8 8.4 8.6 8.2 10.0 10.6 9.2 9.4 9.3 9.5 13.7 13.8 13.6

40-44 8.0 8.3 7.6 7.2 7.4 7.0 8.7 9.3 8.1 8.0 7.9 8.0 11.5 11.4 11.5
45-49 6.9 7.1 6.6 6.3 6.5 6.0 7.5 7.8 7.1 6.8 6.9 6.8 9.5 9.5 9.6
50-54 5.9 6.0 5.8 5.4 5.5 5.3 6.5 6.8 6.2 6.1 6.0 6.2 8.0 7.9 8.0
55-59 5.0 5.1 5.0 4.6 4.6 4.5 5.6 5.7 5.5 5.4 5.3 5.4 6.6 6.5 6.7
60-64 4.3 4.3 4.3 3.9 4.0 3.9 4.9 4.9 4.8 4.6 4.5 4.7 5.6 5.6 5.6
65-69 3.6 3.6 3.6 3.3 3.3 3.3 4.1 4.2 4.0 3.9 3.8 4.0 4.8 4.8 4.9
70-74 3.1 3.0 3.1 2.9 2.8 2.9 3.4 3.5 3.4 3.3 3.1 3.5 4.0 3.9 4.1
75-79 2.6 2.6 2.6 2.5 2.5 2.5 2.9 2.9 2.8 2.8 2.6 2.9 3.4 3.4 3.4
80-84 2.2 2.2 2.2 2.1 2.1 2.1 2.4 2.5 2.4 2.4 2.3 2.4 2.8 2.7 2.9
85+ 1.8 1.7 1.8 1.7 1.7 1.7 1.9 1.9 2.0 1.9 1.8 1.9 2.2 2.2 2.2
Expected Remaining Liftimes (Year) of the General US Population, and of Prevalent Dialysis and transplant
Patients, by Race and Gender from the 2004 USRDS Annual Data Report

Transplant, 2002
All Races White Black Native American Asian
Age All M F All M F All M F All M F All M F
0-14 49.5 49.7 49.2 50.3 50.6 50.0 45.4 45.7 44.8 38.8 39.4 38.0 57.1 56.2 58.6
15-19 39.3 39.3 39.6 39.8 39.8 40.0 36.5 36.5 36.5 33.7 34.1 33.4 46.5 45.5 48.1
20-24 35.6 35.5 35.9 36.0 35.9 36.3 33.0 33.0 33.2 31.2 31.5 30.9 42.7 41.6 44.3
25-29 31.9 31.7 32.3 32.2 32.1 32.6 29.7 29.5 29.9 28.6 29.0 28.4 38.8 37.6 40.5
30-34 28.4 28.1 28.9 28.6 28.4 29.2 26.4 26.2 26.8 26.2 26.3 26.2 34.9 33.7 36.8
35-39 25.0 24.6 25.7 25.2 24.9 25.9 23.2 22.8 23.8 23.7 23.5 24.2 31.1 29.8 33.1

40-44 21.8 21.3 22.8 22.1 21.6 23.0 20.1 19.6 20.7 21.4 20.9 22.1 27.4 26.0 29.5
45-49 19.0 18.4 20.0 19.2 18.7 20.3 17.3 16.8 18.0 19.1 18.6 19.9 23.8 22.5 25.9
50-54 16.4 15.8 17.5 16.7 16.1 17.8 14.7 14.3 15.5 17.0 16.5 17.7 20.6 19.4 22.6
55-59 14.0 13.4 15.1 14.2 13.6 15.4 12.4 11.9 13.2 15.2 14.7 16.0 17.6 16.4 19.6
60-64 11.8 11.2 12.9 12.0 11.4 13.1 10.5 9.9 11.3 13.8 13.2 14.7 14.9 13.8 16.9

65-69 9.9 9.3 11.1 10.0 9.4 11.2 8.8 8.2 9.8 12.6 11.8 13.8 12.8 11.7 14.7
70-74 8.3 7.7 9.6 8.3 7.7 9.6 7.4 6.7 8.6 11.3 10.5 12.5 10.9 9.9 12.9
75-79 7.3 6.8 8.5 7.3 6.8 8.5 6.7 5.9 7.9 10.8 10.0 12.2 9.8 9.0 11.6
 Transition Points for Modality Transfers

Peritoneal Dialysis Transfer to Hemodialysis :

Recurrent infection
Catheter malfunction
Ultrafiltration failure
Adequacy (solute) failure
Psychological burnout
Activities of daily living failure
Hospitalization/surgery
Uncontrolled diabetes
Bond composition morbidity delta

Hemodialysis Transfer to Peritoneal Dialysis

Recurrent congestive heart failure

Access failure (steal, recurrent [3], lower extremity, option)
Hypercoagulability
Malnutrition
Intradialysis hypotension
Nursing home care
 Proposed Criteria for
Initiation of Renal Replacement Therapy

Oliguria (urine output < 200 mL/12 hr)

Anuria or extreme oliguria (urine output <50 mL/12 hr)
Hyperkalemia ([K*] > 6.5 mmol/L)
Severe acidemia (pH , 7.1)
Azotemia ([urea] > 30 mmol/L)
Clinically significant organ (especially lung) edema
Uremic encephalopathy
Uremic pericarditis
Uremic neuropathy/myopathy
Severe dysnatremia ([Na] > 160 or < 115 mmol/L)
Deug overdose with dialyzable toxin
DefiningTherapies for Acute Renal Failure in Patients with Chronic
Kidney Disease
Therapy Definition
Hemodialysis (HD) Convective-based process
across semipermeable
membrane
Hemofiltration Convective-based solute
removal with plasma water
filtered across highly
permeable membrane
Ultrafiltration (UF) Plasma water removal, 2 to 5
L/24 hr
Sustained low Slow, convective-based
efficiency dialysis process across
semipermeable membrane
Peritoneal dialysis Diffusive and convective
(PD) transport across peritoneal
membrane
Indication Modality Option
Solute/H2O removal IHD, DHD, CAVHD
Hyperkalemia CVVHD
Volume control, acid-base IHD, CVVH, CAVH
disorders, azotemia,
congestive heart failure,
multiple organ failure
SCUF, CVVUF, IUF
Fluid removal, congestive
heart failure, total body
anasarca, intubation or re-
intubation risk
IHD treatment failure due to SLED
hypotension or inadequate
clearance
CAPD, CCPD (APD)
Azotemia, volume control,
hypotension, withaout access
to continuous hemodialysis
treatments
 KEY POINTS : CHRONIC RENAL FAILURE
The National Kidney Foundation developed and published clinical practice
guidelines for CKD in 2002 to more consistently diagnose and treat CKD and
its comorbidities
At a set point (usually > 50% reduction in GFR), a relentless progressive loss
of renal function ensues even when the initial insult becomes inactive: the
hyperfiltration hypothesis.
Progression of renal insufficiency involves hemodynamic and
nonhemodynamic mechanisms.
ACE inhibitors are the most effective agents in slowing the progression of
renal disease by both hemodynamic and nonhemodynamic mechanisms.
The most common causes of CKD are diabetes and hypertension.
Comorbidities associated with CKD need treatment to optimize survival and
diminish morbidity. This includes managing hypertension, blood lipids,
smoking cessation, target weight, anemia, and glycemic control.
Major surgical interventions mandate thorough medical evaluation, particularly
cardiovascular health. The best cardiac noninvasive screening assessment is
a dobutamine echocardiogram.
 Pathophysiology of ischemic acute renal failure.

Renal ischemia and reflow

Persistent cell hypoxia

Persistant disruption
of actin microfilaments

Loss of cell Brush border Impaired cell-cell and Impaired tight

polarity loss cell-matrix adhesion juntion function

Redistribution of Na+, Shedding of brush Detachment and

K+-ATPase to epical border debris into exfoliation of cells
membrane domain the tubules
Loss of
continuity of
renal epithelium

Cell-cell adhesion
In the
and aggregation
presence
of

Intratubule cast
Increased intratubule pressure
formation
Impaired solute and
water transport
Obstruction Back-leakage
of filtrate
The pathophysiology of reperfusion injury. The generation of reactive oxygen species.

ISCHEMIA REPERFUSION

ATP DEPLETION Accumulation of Xanthine

hypoxanthine

Increase in cytosolic
Ca2+ Xanthine
oxidase Superoxide
generation
Activation of calmodulin-dependent protease

Hydrogen
Xanthine Peroxida
dehydrogenase Fe2+
Fenton reaction

Fe3+
Hydroxyl radical

OXIDANT INJURY
 Algorithm for the differential diagnosis of acute renal failure.

Acute renal failure

(increased BUN/creatinine)

Compaire to Assess volume states Check patency of Review nephrotoxic

pre-op labs (exam, weights, CVP, PCWP catheters/stents exposure

Optimized

Resolved No resolution

Pre-renal ARF
Renal U/S
R/O extravasation

Non obstruction Obstruction Leak

Urinalysis,
urinary indices Post renal ARF

ATN
 Urinary indices

UNa x V
Fractional Excretion
= Ucreat x V x 100%
of Sodium
Pcreat
( FENa)

Renal Failure Index UNa x Pcreat

( RFI) =
Ucreat
 Kidney injury mosaic for progressive renal failure
Initial kidney Decrease in Neurogenic response
injury functional
renal mass

Angiotensin II
Nitric oxide
Injury Sympathetic nervous system (SNS)
REMODELING
EVENTS

Glomerular epithelial
endothelial, mesangial
STRUCTURAL
Smooth muscle cells
ALTERATIONS
Extracellular matrix (ECM)
Podocyte denudation
Hypoxia injury hypothesis
Proteinurea
Lipid injury
Glomerular hypertension
Vasoconstrictor/vasocilator
Fibrogenic
Proliferative
REGULATORY
ECM proteins
SUBSTANCES
Collagen promoters/proteases
Apoptotic lethal/survival
Proinlammatory chemoattractant
ACE gene (D/I)
Genetics regulators C-met gene
Quantitative trait locus (QTL)
Altered gene expression

MECANISM OF PROGRESSION
Renoprotective Intervention regimens
Interstitial Increase collagen deposition
Glomerulosclerosis
fibrosis Decrease ECM degradation
Increase metalloproteinase inhibitor
End-Stage Disease (ESRD)
 Prognosis of acute tubular necrosis

Death
50%

Acute Renal Failure

25% Complete 20% Incomplete 5% No

Recovery Recovery Recovery

15% Function 5% Function

Stable Regresses
 Optimization of kidney disease care

Early detection of CRF

Intervebtions that Prevention of uremic Modification of Preparation of renal

delay progression complications comorbidity replacement therapy

ACE inhibitors Malnutrition, abnormal Diabetes disease Renal disease

body composition control education

BP control Osteodystrophy Vascular disease Modality selection

peripheral/central

Blood sugar regulation anemia Cardiac disease Timely acces

placement

Hyperlipidemia control Hypervolemia/edema Pulmonary disease Timely dialysis initiation

? Protein restriction acidosis Dialysis intake

completion
Algorithm for blood pressure management in chronic kidney disease

Lifestyle modifications
Step 1
achieve dry weight

Not at goal BP
(BP > 140/90 mm Hg)

Step 2 Initial drug choices

Hypertension without Hypertension with

compelling indications compelling indications

Stage 1 Hypertension Stage 2 Hypertension Drugs for

(BP > 140-159/90-99 mm Hg) (BP > 160/100 mm Hg) the compelling
start an ACEI or ARB start a 2-drug combination indications
(usually an ACEI or ARB and
a CCB

Not a goal BP

Step 3 Add a -blocker or clonidine

Work-up for secondary causes

Step 4
if W/u neg. add minoxidil
 Kidney disease continouum

TX
ICHD
HHD
TX evaluation
PD
and planned
access
reno-
placement
protective TX
strategies PD+HD
HHP PD
ICHP Transition IHD
PD points

ESRD Treatment options

Initiate
CKD assessment Late
dialysis Continuing care

Nurse educator Modality Achieve K/DOQI targets Monthly visit Treatment

Patient life plan selection nutrition : SGA Acute visits withdrawal
social worker : SF 36 Post hospitalization
Acute transition points