ALL ABOUT

CKD AND AKI

dr.

Urology Department
Faculty of Medicine – RSHS
Bandung 2021
Acute Kidney Injury
 Definition
Sudden impairment of kidney function resulting in the retention of nitrogenous and other waste product
normally cleared by the kidneys.
An acute rise in serum creatinine (SCr) and/or an acute decline in urine output.

(KDIGO)
AKI is defined as any of the following (Not Graded):
● Increase in SCr by >0.3 mg/dl (>26.5 lmol/l) within 48 hours; or
● Increase in SCr to >1.5 times baseline, which is known or presumed to have occurred within the
prior 7 days; or
● Urine volume <0.5 ml/kg/h for 6 hours

Harrison's Principles of Internal Medicine 20th edition. New York: McGraw-Hill, Health Professions Division.
KDIGO Clinical Practice Guideline for Acute Kidney Injury
 Etiology and Pathophysiology

The causes of AKI have been

divided into three broad categories:
● Prerenal azotemia
● Intrinsic renal parenchymal
disease
● Postrenal obstruction

Harrison's Principles of Internal Medicine 20th edition. New York: McGraw-Hill, Health Professions Division.
 Postrenal obstruction
Occurs when the normally
unidirectional flow of urine is
acutely blocked either
partially or totally, leading to
increased retrograde
hydrostatic pressure and
interference with glomerular
filtration.

Prerenal Azotemia Intrinsic renal parenchymal

Rise in SCr or BUN concentration disease
due to inadequate renal plasma The most common causes are
flow and intraglomerular sepsis, ischemia and
hydrostatic pressure to support nephrotoxins, both endogenous
normal glomerular filtration. and exogenous.

Harrison's Principles of Internal Medicine 20th edition. New York: McGraw-Hill, Health Professions Division.
 Diagnostic Evaluation

● History
● Physical examination
● Urine findings
● Blood laboratory findings
● Renal failure indices
● Radiologic evaluations
● Renal biopsy
● Novel biomarkers
The gold standard for evaluating
kidney function is a measurement of
GFR using a marker of pure
glomerular filtration.

Harrison's Principles of Internal Medicine 20th edition. New York: McGraw-Hill, Health Professions Division.
Harrison's Principles of Internal Medicine 20th edition. New York: McGraw-Hill, Health Professions Division.
Harrison's Principles of Internal Medicine 20th edition. New York: McGraw-Hill, Health Professions Division.
 Classification

In Wein, A. J., In Kavoussi, L. R., Campbell, M. F., & Walsh, P. C. (2012). Campbell-Walsh urology. Chicago (Author-Date, 15th ed.) Wein, Alan J., Louis R.
 Management

Harrison's Principles of Internal Medicine 20th edition. New York: McGraw-Hill,

Health Professions Division.
 Complication
● Uremia
● Hypervolemia and hypovolemia
● Hyponatremia
● Hyperkalemia
● Acidosis
● Hyperphosphatemia and hypocalcemia
● Bleeding
● Infections
● Cardiac complications → arrhythmias, pericarditis, and pericardial effusion
● Malnutrition

Harrison's Principles of Internal Medicine 20th edition. New York: McGraw-Hill, Health Professions Division.
 Prognosis
● The development of AKI is associated with a significantly increased risk of in-hospital and long-
term mortality, longer length of stay, and increased costs.
● Prerenal azotemia, with the exception of the cardiorenal and hepatorenal syndromes, and postrenal
azotemia carry a better prognosis than most cases of intrinsic AKI.
● The kidneys may recover even after severe, dialysis-requiring AKI.
● Survivors of an episode of AKI requiring temporary dialysis, however, at extremely high risk for
progressive CKD, and up to 10% may develop end-stage renal disease.

Harrison's Principles of Internal Medicine 20th edition. New York: McGraw-Hill, Health Professions Division.
Chronic Kidney
Disease
 Definition
The persistence of structural or functional abnormalities of the kidney for more than 3 months. (Campbell)

Etiology
● Younger children : CAKUT (Renal hypoplasia/dysplasia)
○ Renal hypoplasia/dysplasia
○ Obstructive lesions : Posterior urethral valves & prune belly syndrome
○ Childhood → Renal cystic diseases : Multicystic kidneys, cystic renal dysplasia, juvenile nephronophthisis,
& autosomal recessive polycystic kidney disease
○ Early childhood → Glomerular diseases : Nephrotic syndrome, focal segmental glomerulosclerosis,
hemolytic uremic syndrome, membranoproliferative glomerulonephritis, membranous nephropathy, &
lupus nephritis
● Adult
○ Iatrogenic
Pathophysiology

● The pathophysiology of CKD involves two broad sets of mechanisms of damage:

a. Initiating mechanisms specific to the underlying etiology (e.g., abnormalities in kidney development or
integrity, immune complex deposition and inflammation in certain types of glomerulonephritis, or toxin
exposure in certain diseases of the renal tubules and interstitium)
b. Hyperfiltration and hypertrophy of the remaining viable nephrons
In Wein, A. J., In Kavoussi, L. R., Campbell, M. F., & Walsh, P. C. (2012). Campbell-Walsh urology. Chicago (Author-Date, 15th ed.) Wein, Alan J., Louis R.
Harrison's Principles of Internal Medicine 20th edition. New York: McGraw-Hill, Health Professions Division.
 Classification of CKD
(based on Kidney Disease Outcomes Quality Initiative Staging System)
Criterias :
- based on decrease in GFR (GFR normal : 40 mL/min/1.73 m2)
- Staging excludes : Patients younger than 2 years of age
- Renal abnormalities persist > 3 months & infants younger than 3 months of age

Complications of CKD
- Nausea & vomiting
- Protein malnutrition : Seen in 20% of pediatric patients in any stage of CKD due to impaired appetite → inadequate
intake → strongly associated with mortality
- Growth impairment : Common complication in children with CKD, experience 1.5 standard deviations below normal
for height.
- Anemia : The most common, due to deficiency of erythropoietin
- Electrolytes abnormalities : Metabolic acidosis, worsen retention of phosphate
In Wein, A. J., In Kavoussi, L. R., Campbell, M. F., & Walsh, P. C. (2012). Campbell-Walsh urology. Chicago (Author-Date, 15th ed.) Wein, Alan J., Louis R.
Harrison's Principles of Internal Medicine 20th edition. New York: McGraw-Hill, Health Professions Division.
 Treatment
1. Slowing the progression of CKD
○ Reducing intraglomerular hypertension & proteinuria
i. The basis for the treatment guideline establishing 130/80 mmHg as a target blood pressure in proteinuric CKD
patients.
ii. The combination of ACE inhibitors and ARBs are effective in slowing the progression of renal failure in patients
with advanced stages of both diabetic and nondiabetic CKD, in large part through effects on efferent
vasodilatation and the subsequent decline in glomerular hypertension.
iii. Among the calcium channel blockers, diltiazem and verapamil may exhibit superior antiproteinuric and
renoprotective effects compared to the dihydropyridines. At
2. Slowing the progression of diabetic retinopathy
3. Managing other complications of CKD
○ Medication dose adjustment
i. Some drugs should be avoided : metformin, meperidine, and oral anti-hyperglycemics that are eliminated by the
kidney.
ii. NSAIDs should be avoided because of the risk of further worsening of kidney function.
iii. Many antibiotics, antihypertensives, and antiarrhythmics may require a reduction in dosage or change in the dose
interval.
iv. Nephrotoxic radiocontrast agents and gadolinium should be avoided

Harrison's Principles of Internal Medicine 20th edition. New York: McGraw-Hill, Health Professions Division.
 Treatment
Peritoneal Dialysis (CAPD, CCPD, both)
Hemodialysis
● In peritoneal dialysis, 1.5–3 L of a dextrose-
Hemodialysis relies on the principles of solute diffusion containing solution is infused into the peritoneal
across a semipermeable membrane. cavity and allowed to dwell for a set period of time,
usually 2–4 h.
There are three essential components to hemodialysis: the
● The clearance of solutes and water during a
dialyzer, the composition and delivery of the dialysate, and peritoneal dialysis exchange depends on the balance
the blood delivery system between the movement of solute and water into the
peritoneal cavity versus absorption from the
peritoneal cavity.

Harrison's Principles of Internal Medicine 20th edition. New York: McGraw-Hill, Health Professions Division.
 Treatment

Renal Replacement Therapy

● Donor : Living and/ deceased
● The current standard of care is that the candidate should have a life expectancy of >5 years to be put on a
deceased organ wait list. Even for living donation, the candidate should have >5 years of life expectancy.
● Donor should be free from : Coronary artery disease, HIV, hepatitis B or C, TB, neoplasm

Maintenance Therapy
● Antimetabolites
● steroids
● Calcineurin inhibitors
● TOR inhibitors
● Belatacept

Harrison's Principles of Internal Medicine 20th edition. New York: McGraw-Hill, Health Professions Division.
 Treatment

Immunosuppressive Treatment

Harrison's Principles of Internal Medicine 20th edition. New York: McGraw-Hill, Health Professions Division.
Harrison's Principles of Internal Medicine 20th edition. New York: McGraw-Hill, Health Professions Division.
 Prognosis

Harrison's Principles of Internal Medicine 20th edition. New York: McGraw-Hill, Health Professions Division.
Hyperkalemia
 Definition

● Hyperkalemia is defined as a plasma potassium level of 5.5 mM, occurring in up to 10% of

hospitalized patients.
● Severe hyperkalemia (>6.0 mM) occurs in approximately 1 %, with a significantly increased risk
of mortality.
● Pseudohyperkalemia
Hyperkalemia should be distinguished from factitious hyperkalemia or "pseudohyperkalemia", an
artifactual increase in serum K+ due to the release of K+ during or after venipuncture.

Harrison's Principles of Internal Medicine 20th edition. New York: McGraw-Hill, Health Professions Division.
 Etiology

Harrison's Principles of Internal Medicine 20th edition. New York: McGraw-Hill, Health Professions Division.
 Diagnostic
Approach

Harrison's Principles of Internal Medicine 20th edition. New York: McGraw-Hill, Health Professions Division.
 Management
The treatment of hyperkalemia is divided into three stages:
1. Immediate antagonism of the cardiac effects of hyperkalemia
10 mL of 10% calcium gluconate (3-4 mL of calcium chloride), infused IV over 2-3 min with
cardiac monitoring. The effect starts in 1 -3 min and lasts 30-60 min.
2. Rapid reduction in plasma K+ concentration by redistribution in to cells
10 units of intravenous regular insulin followed immediately by 50 mL of 50% dextrose, the effect
begins in 10-20 min, peaks at 30-60 min, and lasts for 4-6 h.
3. Removal of potassium
This is typically accomplished using cation exchange resins, diuretics, and/or dialysis.
Hemodialysis is the most effective and reliable method to reduce plasma K+ concentration.

Harrison's Principles of Internal Medicine 20th edition. New York: McGraw-Hill, Health Professions Division.
Urethroplasty
 Urethroplasty
● Urethroplasty is an open surgical reconstruction or replacement of the urethra that has been narrowed by scar tissue
and spongiofibrosis (urethral stricture).
● Urethroplasty is the gold standard for urethral reconstruction with the best and most durable results.

URETHROPLASTY PROCEDURE

1. Excision and primary anastomosis (EPA) urethroplasty

○ A short segment of the bulbar urethra (between the scrotum & prostate) is excised and the cut ends of the
urethra are sewn back together.
2. Graft urethroplasty
○ A piece of tissue, typically from the extra-genital skin or from the inner lining of the mouth (buccal graft), is
used as a patch to increase the size of the urethra.
3. Penile flap urethroplasty
○ A flap of penile skin is used to patch a urethral stricture.
4. Staged Urethroplasty
○ The scarred urethra is surgically removed and replaced with a buccal or skin graft. This replaced urethra heals
over the course of a few months; once the graft is healed, a second surgery forms the graft into a tube to
reconstruct the urethra.

Textbook of Male Genitourethral Reconstruction by Francisco E. Martins, Sanjay B. Kulkarni, Tobias S. Köhler.
 Urethroplasty
● Indications include:
○ Strictures related to lichen sclerosis (LS)
○ Prior reconstructive surgery for hypospadias or urethral stricture
○ Poor tissue quality or a paucity of viable genital skin for flap reconstruction
○ An absent lumen precluding substitution urethroplasty.

PREOPERATIVE EVALUATION

● Adequate preoperative counsel and surgical planning

● Evaluation :
○ History : a detailed history with specific attention to pertinent pediatric urological history, prior surgical
interventions, previous history of genitourinary trauma or infection, recent urethral instrumentation, current
voiding pattern, and a history of urinary retention, presence of urinary incontinence, erectile dysfunction or
chordee, history of malignancy and relevant treatment modalities used (especially radiation), and oral pathology
or tobacco use.
○ Physical examination : Documentation of quality and availability of penile skin and soft tissue, circumcision
status, location and severity of genital scars, and the presence of LS.
○ Radiographic : Retrograde urethrogram (RUG) with or without cystourethrogram (VCUG) → understand
stricture length, location & other urethral or bladder abnormalities
Textbook of Male Genitourethral Reconstruction by Francisco E. Martins, Sanjay B. Kulkarni, Tobias S. Köhler.
 Remember
● Between the first and second stage : A period of 4–6 months is typical for graft take and stabilization, and the patient needs to
understand the process of sitting to void through a penile or upper scrotal urethrostomy during this time.
● Sexual intercourse is allowed approximately 6–8 weeks after the first procedure, and the patient is made aware that semen will
also emanate from the urethrostomy.
● The second stage procedure : a catheter or urethral stent is left in the urethra for a period of 18–21 days to permit urinary
diversion and urethral healing. Intercourse is again allowed after 6–8 weeks.

Textbook of Male Genitourethral Reconstruction by Francisco E. Martins,

Sanjay B. Kulkarni, Tobias S. Köhler.
 Surgical Technique: First Stage for Penile Stricture

(a) Complex first stage hypospadias patient with proximal dorsal buccal mucosa graft seen between forceps at proximal urethrostomy; ( b) Proximal dorsal graft at urethrostomy
opening for extensive LS stricture; (c) Closer view of urethrostomy and graft

Textbook of Male Genitourethral Reconstruction by Francisco E. Martins, Sanjay B. Kulkarni, Tobias S. Köhler.
 Surgical Technique: Second Stage for Penile Stricture

Textbook of Male Genitourethral Reconstruction by Francisco E. Martins, Sanjay B. Kulkarni, Tobias S. Köhler.
 Predictors of Urethral Stricture
Recurrence after Urethroplasty

Textbook of Male Genitourethral Reconstruction by Francisco E. Martins, Sanjay B. Kulkarni, Tobias S. Köhler.
 Substitution
Urethroplasty for
Bulbar Urethral
Strictures

Textbook of Male Genitourethral Reconstruction by Francisco E. Martins, Sanjay B. Kulkarni, Tobias S. Köhler.
 Ventral Onlay Surgical Technique for Bulbar Strictures

Fig. 16.2 Ventral onlay. (a) The corpus spongiosum is opened along its ventral surface and (b) the urethral lumen is fully exposed, extending the urethrotomy distally and proximally
to the stenosis. (c) The graft is sutured to the edge of the urethral mucosa plate. (d) The spongiosum tissue is closed over the graft. (e) Schematic image of ventral onlay

Textbook of Male Genitourethral Reconstruction by Francisco E. Martins, Sanjay B. Kulkarni, Tobias S. Köhler.
 Dorsal Onlay Surgical Technique for Bulbar Strictures

Fig. 16.3 Dorsal onlay. (a) The bulbar urethral is circumferentially mobilized and rotated. (b) The dorsal urethral surface is incised along the midline to expose the entire stricture. (c)
The graft is spread, fixed over the corpora cavernosa. (d) The bulbar urethra is rotated back and the margin of the graft is sutured to the margin of the urethral mucosal plate. (e)
Schematic image of dorsal onlay

Textbook of Male Genitourethral Reconstruction by Francisco E. Martins, Sanjay B. Kulkarni, Tobias S. Köhler.
 Lateral Onlay Surgical Technique

Fig. 16.4 Lateral onlay. (a) The urethra is mobilized from the albuginea only along the left side. (b) The dorso- lateral side of the urethra is incised longitudinally. (c) The graft is
sutured to the underlying albuginea, and the right margin of the graft is sutured to the left margin of the urethral plate (d) and on the other side. (e) Schematic image of lateral onlay

Textbook of Male Genitourethral Reconstruction by Francisco E. Martins, Sanjay B. Kulkarni, Tobias S. Köhler.
 Dorsal Inlay Surgical Technique

Fig. 16.5 Dorsal inlay. (a) The urethra is left adherent to the corpora cavernosa and is longitudinally opened ventrally extending to the distal and proximal healthy urethra. (b) The
strictured urethral plate is longitudinally opened dorsally. (c) The graft is sutured to the margins of the urethral plate and fixed to the corpora cavernosa. (d) The urethra is
retubularized over a urethral catheter. (e) Schematic image of dorsal inlay

Textbook of Male Genitourethral Reconstruction by Francisco E. Martins, Sanjay B. Kulkarni, Tobias S. Köhler.
 Augmented Anastomotic Urethroplasty

Fig. 16.6 Augmented anastomotic urethroplasty. (a) The bulbar urethra is circumferentially mobilized and a tight stricture is completely removed. (b) Both proximal
and distal urethral walls are dorsally spatulated (c) and sutured to the graft fixed over the corpora cavernosa. (d) The ventral side of the urethra is then closed. (e)
Schematic image of augmented anastomotic urethroplasty

Textbook of Male Genitourethral Reconstruction by Francisco E. Martins, Sanjay B. Kulkarni, Tobias S. Köhler.
 Two-sided Dorsal plus Ventral Double Graft

Fig. 16.7 Two-sided dorsal plus ventral double graft. (a) Combination of dorsal inlay (arrow) and ventral onlay (arrow head). Schematic image is shown in (c). (b) Combination of
dorsal onlay (arrow) and ventral inlay (arrow head). Schematic image is shown in (d)

Textbook of Male Genitourethral Reconstruction by Francisco E. Martins, Sanjay B. Kulkarni, Tobias S. Köhler.
 Surgical Reconstruction of Failed Anterior Urethroplasty

Pendulous
Urethra

Fig. 18.7 Urethral plate salvage with overlapping dorsal and ventral buccal mucosa grafts. (a) Inadequate distal urethral
plate (blue line) for primary graft ventral onlay, (b) Urethral plate incision and dorsal buccal mucosa graft inlay, (c)
Combined with ventral buccal mucosa graft onlay, (d) Completion of ventral graft anastomosis with healthy surrounding
spongiosal tissue (asterisk∗) for primary closure

Textbook of Male Genitourethral Reconstruction by Francisco E. Martins, Sanjay B. Kulkarni, Tobias S. Köhler.
 Surgical Reconstruction of Failed Anterior Urethroplasty

Bulbar
Urethra

Fig. 18.9 Loop perineal urethrostomy via midline perineal incision (a)
preservation of the posterior urethral plate and antegrade blood supply
through the corpora spongiosum after complete bulbar mobilization with 5 cm
Fig. 18.8 Recurrent mid to proximal 4 cm bulbar urethral stricture
urethrostomy, (b) z-plasty advancement skin flap closure posterior to loop
following penile skin graft (a) reconstructed with complete excision and
urethrostomy to reduce skin tension
reanastomosis (b and c), preoperative stretched penile length 17.5 cm (d)

Textbook of Male Genitourethral Reconstruction by Francisco E. Martins, Sanjay B. Kulkarni, Tobias S. Köhler.
 Static and Dynamic
Component of Bladder
BPH may cause physical compression of the urethra and result in anatomic
bladder outlet obstruction (BOO) through two mechanisms:
● Static component
Attributed to the anatomic obstruction resulting from bulk
enlargement of the prostate → under the regulation of androgens
● Dynamic component
Mediated by the tension of prostate smooth muscle via α-
adrenoceptors. Increased adrenergic nervous system and prostatic
smooth muscle tone.

Both mechanisms increase resistance to urinary flow at the level of the

bladder outlet.

Lepor H. Pathophysiology of benign prostatic hyperplasia: insights from medical therapy for the disease. Rev Urol [Internet]. 2009;11(Suppl 1):S9–13. Available from:
http://www.ncbi.nlm.nih.gov/pubmed/20126609%0Ahttp://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC2812891
Patel ND, Parsons JK. Epidemiology and etiology of benign prostatic hyperplasia and bladder outlet obstruction. Indian J Urol. 2014;30(2):170–6.
 The static component leading
to urethral compression.

The dynamic component.

The bladder outlet and prostate
are richly supplied with alpha-
1 receptors (blue dots), which
increase smooth muscle tone,
promoting obstruction to the
flow of urine.

Patel ND, Parsons JK. Epidemiology and etiology of benign prostatic hyperplasia and bladder outlet obstruction. Indian J Urol. 2014;30(2):170–6.
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