1

welcome

SEMINAR ON RENAL FAILURE

BY FASIL : WAGNEW (BSC, MSC )

september 22/2016

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Presentation out line(AKI &CKD)Definition

Epidemiology

Aetiology

Pathogenesis

Pathophysiology

Clinical features

Differential diagnosis

Diagnostic modalities

Medical and/or surgical management

Evidence based nursing interventions  

september 22/2016

Seminar objective

At the end of this session,we will be ….Define and Identify the cause of AKI and CKDExplain the clinical feature of AKI and CKDIdentify the diagnostic modality of renal failureDescribe the treatment option for renal failure

and ESRDApply evidence based nursing intervention

september 22/2016 3

4BY FASIL:WA

september 22/2016

6september 22/2016

7september 22/2016

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Acute Kidney Injury

september 22/2016

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Definition

It is a Rapid deteriotion of renal function resulting in

retention of nitrogenous wastes and inability of kidney to

regulate fluid and electrolyte homeostasis. Nelson 20 ed

september 22/2016

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pRIFLE, AKIN, and KDIGO

• AKI incidences across the cohort according to pRIFLE, AKIN, and KDIGO were 51.1%, 37.3%, and 40.3%.Mortality was higher among patients with AKI across all definitions (pRIFLE, 2.3%; AKIN, 2.7%; KDIGO, 2.5%;P,0.001 versus no AKI [0.8%–1.0%](Scott M. Sutherland et.al,2015).

• Despite the above definition criteria Research has identified improved biomarkers of acute kidney injury (AKI). Cystatin C (CysC) is a better glomerular filtration rate marker than serum creatinine (SCr) and may improve AKI definition (Zappitelli et al,2015)

september 22/2016

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Epidemiology of AKI in world

A systematic review (2004–2012) of large cohort studies was conducted to estimate the world incidence of AKI and its stages.“Among the 154 studies (n=3,585,911) that adopted a KDIGO-equivalent AKI definition, the pooled incidence rates of AKI were 21.6% in adults (95% confidence interval [95% CI], 19.3 to 24.1) and 33.7% in children (95% CI, 26.9 to 41.3). The pooled AKI-associated mortality rates were 23.9% in adults (95% CI, 22.1 to 25.7) and 13.8% in children (95% CI, 8.8 to 21.0)”. (Paweena S.et.al,2013).september 22/2016

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World Incidence of AKI: A Meta-Analysis Paweena Susantitaphong,*†‡ Dinna N. Cruz,§ Jorge Cerda,‖ Maher Abulfaraj,* Fahad Alqahtani,* Ioannis

Koulouridis,*† and Bertrand L. JaberBackground and objectivesThe burden of AKI around the globe has not been systematically examined.Design, setting, participants, & measurements A systematic review (2004–2012) of large cohort studies was conducted to estimate the world incidence

of AKI and its stages of severity and associated mortality, and to describe geographic variations according to countries, regions, and their economies. AKI definitions were reclassified according to the Kidney Disease Improving Global Outcomes (KDIGO) staging system. Random-effects model meta-analyses and meta-regressions were used to generate summary estimates and explore sources of heterogeneity.

Results There were 312 studies identified (n=49,147,878) , primarily in hospital settings. Most studies originated

from North America, Northern Europe, and Eastern Asia, from high-income countries, and from nations that spent ≥5% of the gross domestic product on total health expenditure. Among the 154 studies (n=3,585,911) that adopted a KDIGO-equivalent AKI definition, the pooled incidence rates of AKI were 21.6% in adults (95% confidence interval [95% CI], 19.3 to 24.1) and 33.7% in children (95% CI, 26.9 to 41.3). The pooled AKI-associated mortality rates were 23.9% in adults (95% CI, 22.1 to 25.7) and 13.8% in children (95% CI, 8.8 to 21.0). The AKI-associated mortality rate declined over time, and was inversely related to income of countries and percentage of gross domestic product spent on total health expenditure.

Conclusions Using the KDIGO definition, 1 in 5 adults and 1 in 3 children worldwide experience AKI during a hospital

episode of care. This analysis provides a platform to raise awareness of AKI with the public, government officials, and health care professionals

september 22/2016

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Epidemiology in developing country • According to J. Prakash et al.,2013.“We studied 2405 (1375

male and 1030 female) cases of AKI in the age range 1–95 (mean: 40.32) years. The incidence of CAAKI 4.14 per1000

• In Ethiopia, Case records of 30 pediatric patients with the diagnosis of acute renal failure (ARF) admitted to Tikur Anbessa Hospital. October 2001were analyzed There were 15 females and 15 males. Three patients had GN, one child had obstructive uropathy. Twenty-three patients had post-diarrheal hemolytic uremic syndrome. The age ranges b/n 0.6 years and 7 years with a median age of 2.2 years. (Shimelis D,Tadesse Y, 2004)

september 22/2016

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1.Pre renal

ETHIOLOGY

2. Intrinsic Renal

3. Post-renal

september 22/2016

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Pre-renal

vomiting, diarrhea, poor fluid intake,

fever, use of diuretics

hemorrhage

cardiac failure

liver dysfunction, or

septic shock

september 22/2016

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Intrinsic renal I. Renal Major vessel obstruction -renal vein thrombosis , renal arterial obstruction, hemolytic uremic

syndrome , HSP , polyarteritis and other vasculitis. II. Glomerular - Acute glomerulonephritis ( post streptococcal , other infections ). III. Acute tubulointerstitial nephritis IV. Acute tubular necrosis - Prolongation of pre-renal insult , intravascular hemolysis , sepsis ,

nephrotoxic agents , multiorgan failure , snakebite etc.

Cited by Up to date 21.2september 22/2016

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Post renal Posterior urethral valvesUreteropelvic junction obstructionUreterovesicular junction obstructionUreterocele  Tumor  UrolithiasisHemorrhagic cystitisNeurogenic bladder

Cited by Up to date 21.2

september 22/2016

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PathogenesisPrerenal AKI, also called prerenal azotemia, is characterized

by

• diminished effective circulating arterial volume, which leads

to inadequate renal perfusion and a decreased GFR.

Evidence of kidney damage is absent.

• If the underlying cause of the renal hypoperfusion is

reversed promptly, renal function returns to normal. If hypo-

perfusion is sustained, intrinsic renal parenchymal damage

can developseptember 22/2016

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Cont…d• Among pre renal cause of AKI Sepsis has long

been recognized as a foremost precipitant of AKI. Sepsis-associated AKI (SA-AKI) portends a high burden of morbidity and mortality in both children and adults with critical illness .

• Sepsis associated-AKI poses significant clinical challenges for clinicians( Alobaidi et al. 2015 January ).

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Intrinsic renal AKI

It is characterized by:-renal parenchymal damage,

including sustained hypoperfusion and ischemia. • Severe and prolonged ischemic/hypoxic injury and

nephrotoxic insult lead to acute tubular necrosis (ATN), seen most often in critically ill infants and children

• According to basile et.al,2014. The primary causes of AKI include ischemia, hypoxia or nephrotoxicity. An underlying feature is a rapid decline in GFR usually associated with decreases in renal blood flow.

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Cont….intrinsic AKI

Tumor lysis syndrome is a specific form of AKI related to

spontaneous or chemotherapy-induced cell lysis in patients with

lymphoproliferative malignancies. This disorder is primarily

caused by obstruction of the tubules by uric acid crystals.

Acute interstitial nephritis is another common cause of AKI

and is usually a result of a hypersensitivity reaction to a

therapeutic agent or various infectious agents

september 22/2016

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pathophysiology

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Postrenal AKI blockage in the urinary tract may cause urine to build up in one or

both kidneys. Over time, this fluid buildup can prevent the normal

flow of urine out of the kidney. Conditions that may lead to postrenal

acute kidney injury

It includes a variety of disorders characterized by obstruction of

the urinary tract.

In neonates and infants, congenital conditions, such as posterior

urethral valves and bilateral Ureteropelvic junction obstruction,

account for the majority of cases of AKI.september 22/2016

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Clinical presentation

Pre renal

There may be history of volume loss from

vomiting, diarrhea, or blood loss and may

present with dehydration , hypotension ,

tachycardia , pallor , and decreased urine

output.september 22/2016

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Renal  Hematuria, edema, and hypertension indicates a

glomerular etiology for AKI.Dysentery, petechiae and pallor- HUSPresence of rash, arthritis might suggest SLEHistory of prolong hypotension or with exposure

to nephrotoxic medication most likely have ATN.Allergic interstitial nephritis should be suspected

with fevers, rash, arthralgia, and exposure to certain medications.

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Post renal

• History of interrupted urinary stream and

palpable bladder or kidney suggest obstructive

uropathy.

• Abdominal colic hematuria and dysuria suggest

urinary tract calculi.

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Diagnosis History and Physical examination:-Obtaining a thorough physical examination is

extremely important when collecting evidence about the etiology of AKI. Skin :- Palpable purpura - Systemic vasculitis Maculo papular rash - Allergic interstitial nephritis Eye :- Evidence of uveitis may indicate interstitial nephritis and necrotizing vasculitis. Ear :- Hearing loss - Alport disease and amino glycoside toxicity Mucosal or cartilaginous ulcerations – Wegener granulomatosis.

Pulmonary system :- Respiratory rate , pattern On Auscultation of lungs crepitations

september 22/2016

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Cont..d

Cardiovascular examination may reveal the following:

Murmurs - Endocarditis

Pericardial friction rub - Uremic pericarditis

Increased jugulovenous distention, S3 - Heart failure

Abdomen

Abdominal or costovertebral angle tenderness - Nephrolithiasis,

papillary necrosis, renal artery thrombosis, renal vein thrombosis

distended bladder – Urinary obstructionseptember 22/2016

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Laboratory investigation

Blood urea and S. creatinine levelSerum electrolyte and C3 level

Urinary indices may be useful in differentiating prerenal AKI from intrinsic AKI. Ultrasound - evaluates renal size, able to detect masses, obstruction, stonesRenal biopsy - Patient in whom the etiology is not identified

Clin J Am Soc Nephrol. 2014 Feb 7september 22/2016

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• Clin J Am Soc Nephrol. 2014 Feb 7; 9(2): 382–394. • Published online 2013 Nov 14. doi: 10.2215/CJN.04840513• PMCID: PMC3913238• Renal Relevant Radiology: Use of Ultrasonography in Patients with AKI• Sarah Faubel,* Nayana U. Patel,† Mark E. Lockhart,‡ and Melissa A. Cadnapaphornchai§

• Author information ► Copyright and License information ►• This article has been cited by other articles in PMC.• Go to:• Summary• As judged by the American College of Radiology Appropriateness Criteria, renal Doppler

ultrasonography is the most appropriate imaging test in the evaluation of AKI and has the highest level of recommendation. Unfortunately, nephrologists are rarely specifically trained in Ultrasonography technique and interpretation, and important clinical information obtained from renal ultrasonography may not be appreciated. In this review, the strengths and limitations of grayscale ultrasonography in the evaluation of patients with AKI will be discussed with attention to its use for (1) assessment of intrinsic causes of AKI, (2) distinguishing acute from chronic kidney diseases, and (3) detection of obstruction. The use of Doppler imaging and the resistive index in patients with AKI will be reviewed with attention to its use for (1) predicting the development of AKI, (2) predicting the prognosis of AKI, and (3) distinguishing prerenal azotemia from intrinsic AKI. Finally, pediatric considerations in the use of ultrasonography in AKI will be reviewed.

september 22/2016

DDX for AKI

Chronic Kidney DiseaseAcute Tubular NecrosisAzotemiaHemolytic Uremic Syndrome in EmergencyHyperkalemiaHypertensive EmergenciesLupus nephritis

september 22/2016 35

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Complication of AKI

Metabolic • Hyponatremia • Hyperkalemia• Hypocalcemia, hyperphosphatemia • Hyperuricamia

Pediatrics lecture note

september 22/2016

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Con..d

Metabolic acidosisCardiovascular

Pulmonary edema CHFHypertension Arrhythmias Pericarditis

Neurologic :- Coma and Seizures Hematologic :-Anemia and Coagulopathies & bleeding diathesis E.T.C

Pediatrics lecture note

september 22/2016

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TREATMENT

Medical Management

• In infants and children with urinary tract obstruction, such as

in a newborn with suspected posterior ureteral valves, a

bladder catheter should be placed immediately to ensure

adequate drainage of the urinary tract.

• however, precautions to prevent iatrogenic infection should

be

september 22/2016

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Maintain fluid

• Determination of the volume status is of critical

importance when initially evaluating a patient with

AKI.

• If there is no evidence of volume overload or

cardiac failure, intravascular volume should be

expanded by intravenous administration of isotonic

saline, 20 mL/kg over 30 min.september 22/2016

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Cont…d

• Determination of the central venous pressure may be helpful if

adequacy of the blood volume is difficult to determine.

• After volume resuscitation, hypovolemic patients generally void

within 2 hr; failure to do so suggests intrinsic or postrenal AKI.

• Hypotension caused by sepsis requires vigorous fluid

resuscitation followed by a continuous infusion of nor -

epinephrine. Nelson 20 edseptember 22/2016

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Cont…d• According to KDIGO Aki Guideline 2012, several

diuretics(Furosemide and mannitol ) have potentially Reno-protective effects that might prevent development of AKI and hasten its recovery. However, diuretics can also be harmful, by reducing the circulating volume excessively and adding a prerenal insult, worsening established AKI. Therefore,

1. We recommend not using diuretics to prevent AKI. 2. We suggest not using diuretics to treat AKI, except in

the management of volume overload.

september 22/2016

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Prowle, J. R. et al. (2014)

september 22/2016

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Fenoldopam vs. low dose Dopamin • A comparison between fenoldopam and low-dose dopamine in early renal dysfunction of critically ill patients*• Brienza, Nicola MD, PhD; Malcangi, Vincenzo MD; Dalfino, Lidia MD; Trerotoli, Paolo MD; Guagliardi, Clementina MD; Bortone, Dora

MD; Faconda, Giuseppe MD; Ribezzi, Mario MD; Ancona, Giovanni MD; Bruno, Francesco MD; Fiore, Tommaso MD• Abstract• Objective: Fenoldopam mesylate is a selective dopamine-1 agonist, with no effect on dopamine-2 and α1 receptors, producing a

selective renal vasodilation. This may favor the kidney oxygen supply/demand ratio and prevent acute renal failure. The aim of the study was to investigate if fenoldopam can provide greater benefit than low-dose dopamine in early renal dysfunction of critically ill patients.

• Design: Prospective, multiple-center, randomized, controlled trial.• Setting: University and city hospital intensive care units.• Patients: One hundred adult critically ill patients with early renal dysfunction (intensive care unit stay <1 wk, hemodynamic stability,

and urine output ≤0.5 mL/kg over a 6-hr period and/or serum creatinine concentration ≥1.5 mg/dL and ≤ 3.5 mg/dL).• Interventions: Patients were randomized to receive 2 μg/kg/min dopamine (group D) or 0.1 μg/kg/min fenoldopam mesylate (group

F). Drugs were administered as continuous infusion over a 4-day period.• Measurements and Main Results: Systemic hemodynamic and renal function variables were recorded daily. The two groups were

well matched at enrollment for illness severity and hemodynamic and renal dysfunction. No differences in heart rate or systolic, diastolic, or mean arterial pressure were observed between groups. Fenoldopam produced a more significant reduction in creatinine values compared with dopamine after 2, 3, and 4 days of infusion (change from baseline at time 2, −0.32 vs. −0.03 mg/dL, p = .047; at time 3, −0.45 vs. −0.09 mg/dL, p = .047; and at time 4, −.041 vs. −0.09 mg/dL, p = .02, in groups F and D, respectively). The maximum decrease in creatinine compared with baseline was significantly greater in group F than group D (−0.53 ± 0.47 vs. −0.34 ± 0.38 mg/dL, p = .027). Moreover, 66% of patients in group F had a creatinine decrease >10% of the baseline value at the end of infusion, compared with only 46% in dopamine group (chi-square = 4.06, p = .04). Total urinary output during drug infusion was not significantly different between groups. After 1 day, urinary output was lower in group F compared with group D (p < .05).

• Conclusions: In critically ill patients, a continuous infusion of fenoldopam at 0.1 μg/kg/min does not cause any clinically significant hemodynamic impairment and improves renal function compared with renal dose dopamine. In the setting of acute early renal dysfunction, before severe renal failure has occurred, the attempt to reverse renal hypoperfusion with fenoldopam is more effective than with low-dose dopamine.september 22/2016

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Treatment of hyperkalemia

In AKI, rapid development of hyperkalemia (> 6 mEq/L)

can lead to cardiac arrhythmia, cardiac arrest, and death

The earliest electrocardiographic change seen in patients with

developing hyperkalemia is the appearance of peaked T

waves.

This may be followed by widening of the QRS intervals, ST

segment depression, ventricular arrhythmias, and cardiac

arrest. Cited by up to date 21.2september 22/2016

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Treatment of hyperkalemia

When the serum potassium value rises to >6.0 mEq/L.

Exogenous sources of potassium (dietary, intravenous

fluids, total parenteral nutrition) should be eliminated.

Sodium polystyrene sulfonate resin (Kayexalate), 1

g/kg, should be given orally or by retention enema.

This resin exchanges sodium for potassium and can

take several hr to take effect.september 22/2016

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Cont….d

A single dose of 1 g/kg can be expected to lower the

serum potassium level by about 1 mEq/L. Resin therapy

may be repeated every 2 hr.

More severe elevations in serum potassium (>7 mEq/L),

especially if accompanied by electrocardiographic

changes, require emergency measures in addition to

Kayexalate.september 22/2016

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Treatment of metabolic acidosis

Mild metabolic acidosis is common in AKI. but, it

rarely requires treatment.

• If acidosis is severe, The acidosis should be corrected

partially by the intravenous route, generally giving

enough bicarbonate to raise the arterial pH to 7.20.

The remainder of the correction may be accomplished

by oral administration of sodium bicarbonate.september 22/2016

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Treatment of hypocalcemia

• It is primarily treated by lowering the serum phosphorus level.

Calcium should not be given intravenously, except in cases of

tetany, to avoid deposition of calcium salts into tissues.

• Patients should be instructed to follow a low-phosphorus diet, and

phosphate binders should be orally administered to bind any

ingested phosphate and increase GI phosphate excretion.

• Low phosphate foods (white bread, crackers, cereals, rice and

pasta)

Up to date 21.2.. september 22/2016

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Treatment of hyponatremia

• It is most commonly a dilutional disturbance that

must be corrected by fluid restriction rather than

sodium chloride administration.

• Administration of hypertonic (3%) saline should be

limited to patients with symptomatic hyponatremia

or those with a serum sodium level <120 mEq/L.

september 22/2016

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Treatment hypertension

It can result from hyper reninemia associated with

the primary disease process and/or expansion of the

extracellular fluid volume and

It is most common in AKI patients with acute

glomerulonephritis or HUS.

Salt and water restriction is critical, and diuretic

administration may be usefulseptember 22/2016

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Cont..d

According to Wuhl E, trivelli A,et .al,2009 “Angiotensin converting

enzyme (ACE) inhibitors (enalapril) and Angiotensin II blockers

(losartan) are the antihypertensive medications of choice in all children

with proteinuria renal disease because of their potential ability to slow

the progression”.

• A short action Isradipine 0.05-0.15 mg/kg/dose, maximum dose 5 mg

qid) may be administered.

• Long acting agents such as calcium channel blockers (amlodipine, 0.1-

0.6 mg/kg/24 hr QD or divided bid)september 22/2016

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Treatment of anemia

The anemia of AKI is generally mild (hemoglobin 9-10 g/dL)

and primarily results from volume expansion (hemodilution).

Children with HUS, SLE, active bleeding, or prolonged AKI

can require transfusion of packed red blood cells if their

hemoglobin level falls below 7 g/dL.

packed red blood cells (10 mL/kg) Slow (4-6 hr) transfusion

for diminishes the risk of hypervolemia

Nelson 20 edseptember 22/2016

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Dietary management of AKI

• Nutrition is of critical importance in children who

develop AKI. In most cases, sodium, potassium,

and phosphorus should be restricted.

• Protein intake should be moderately restricted

while maximizing caloric intake to minimize the

accumulation of nitrogenous wastes.september 22/2016

Nutrition• The recommended energy provide target of 20–30

kcal/kg/day and a protein target of 1.5 g/kg/day, in the absence of RRT. In case of RRT, an increase in protein supply including glutamine and micronutrients are suggested [Fiaccadori E, Parenti E,2008].

• According to KDIGO 2O12 guideline recommendations have proposed the following protein intake depending on the age of children presenting with AKI:

2–3 g/kg/day from 0 to 2 years, 1.5–2 g/kg/day from 2 to 13 years, 1.5 g/kg/day above 13 years.

september 22/2016 Thyophiline and renal dysfun

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Indications for dialysis :

1. Anuria/ oliguria

2. Volume overload with evidence of hypertension and/or

pulmonary edema refractory to diuretic therapy

3. Persistent hyperkalemia

4. Severe metabolic acidosis unresponsive to medical management

5. Uremia

6. Blood urea nitrogen >100-150 mg/dL

7. Calcium: phosphorus imbalance, with hypocalcemic tetany that

cannot be controlled by other measuresseptember 22/2016

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Chronic Kidney Disease

september 22/2016

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Chronic kidney disease Patient has CKD if either of the following criteria are

present:1. Kidney damage for ≥3 mo, as defined by structural or

functional abnormalities of the kidney, with or without decreased GFR, manifested by 1 or more of the following features:

– Abnormalities in the composition of the blood or urine– Abnormalities in imaging tests– Abnormalities on kidney biopsy

2. GFR <60 mL/min/1.73 m2 for ≥3 mo, with or without the other signs of kidney damage described above

National Kidney Foundation K/DOQI(2002)september 22/2016

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STANDARDIZED TERMINOLOGY FOR STAGES OF CHRONIC KIDNEY DISEASE (K/DOQI(2002)

september 22/2016

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Etiology

• Result of congenital, acquired, inherited, or metabolic

renal disease.

in children <5 yr old is

– most commonly a result of congenital abnormalities such as

renal hypoplasia, dysplasia, or obstructive uropathyAfter 5 yr of age

acquired diseases (various forms of glomerulonephritis including lupus nephritis) and inherited disorders ( Alport syndrome) predominate.

september 22/2016

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Epidemiology• The incidence and prevalence of all stages of CKD

in children continues to increase worldwide. The kidney replacement therapy incidence rate among 0–19 years of age rose 15 per million population in children (Cynthia J.Wong,2012).

• According to coca et.al,2012 evaluating long-term renal outcomes and non-renal outcomes in patients with AKI. Patients with AKI had higher risks of developing CKD (pooled adjusted hazard ratio 8.8, 95% CI 3.1-25.5), ESRD (pooled adjusted HR 3.1, 95% CI 1.9-5.0)

september 22/2016

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PATHOGENESIS

• In addition to progressive injury with ongoing structural or metabolic genetic diseases, renal injury can progress despite removal of the original insult.

Hyper filtration injuryProteinuriahypertensionHyperphosphatemiaHyperlipidemia

september 22/2016

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Clinical Manifestations

• The clinical presentation of CKD is varied and depends on the underlying renal disease–Children and adolescents with CKD can

present with – edema, –hypertension, –hematuria, and –proteinuria

september 22/2016

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Cont….d

• Infants and children with congenital disorders such as –renal dysplasia and obstructive uropathy

can present in the neonatal period with failure to thrive, polyuria, dehydration, urinary tract infection, or overt renal insufficiency

september 22/2016

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Diagnosis

On P/E:-Pallor and a sallow appearance.– short stature and the bony abnormalities of renal

osteodystrophy (length/height-for age <3rd percentile).

– Children with CKD due to chronic glomerulonephritis (edema, hypertension and fluid overload).

Laboratory Findings(Elevated BUN and serum creatinine, hyperkalemia, hyponatremia, hypernatremia Acidosis, hypocalcemia, hyperphosphatemia, and an elevation in uric acid, hypoalbuminemia, hematuria and proteinuria.

september 22/2016

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Differential diagnosis

Acute kidney injury InjuryAlport SyndromeGlomerulonephritisDiabetic NephropathyGood pasture SyndromeObstractive uropathyNephrolithiasis

UP TO DATE 21.1

september 22/2016

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Management

GENERAL PRINCIPLES – Treat reversible kidney dysfunction • Prevent or slow the progression of kidney

disease – Treat the complications of CKD

– Identify and adequately prepare the child/family in

whom renal replacement therapy will be required

september 22/2016

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REVERSIBLE KIDNEY DYSFUNCTION

Prevent or treat Decreased kidney perfusion from

• Hypotension (eg, septic shock), Volume depletion

from vomiting, diarrhea, diuretic use, or bleeding, and

• the administration of drugs that lower the kidney

perfusion

• Avoid Administration of nephrotoxic drugsseptember 22/2016

69

Blood pressure control

• volume overload glomerular disease salt-restricted diet (2-3 g/24 hr) and can benefit from diuretic therapy

• hydrochlorothiazide 2 mg/kg/24 hr divided bid for CKD stages 1-3.furosemide 1-2 mg/kg/dose bid stage 4 CKD (nelson textbook, 2015)

• According yan li et.al,2016, the combination of a CCB and an ACEI should be a preferable antihypertensive therapy in patients with CKD, considering their higher effect in decreasing blood pressure

september 22/2016

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Meta-analysisAbstractBackground: The renoprotective effect of inhibitors of renin-angiotensin system (RAS) has been

identified through placebo-controlled trials. However, the effect of calcium-channel blockers (CCBs) on renal system is still controversial. Our current meta-analysis includes available evidences to compare the effect of dihydropyridine CCBs and ACEIs or ARBs on renal outcomes and mortality. We also further investigate whether CCBs can be used in combination with inhibitors of RAS to improve the prognosis of patients with chronic kidney disease (CKD).

Methods and results: Electronic databases were searched up to July 2012, for clinical randomized controlled trials, assessing the effect of dihydropyridine CCBs on the incidence of end-stage renal disease (ESRD) and all-cause mortality in contrast to ACEIs or ARBs. Eight clinical trials were included containing 25,647 participants. ESRD showed significantly higher frequency with CCBs therapy compared with ACEIs or ARBs therapy, though blood pressure was decreased similarly in both groups in every trial (OR, 1.25; 95% CI, 1.05–1.48; p = 0.01). In contrast, there was no significant difference in the incidence of all-cause mortality between these two groups, though ACEIs or ARBs exhibited better renoprotective effect compared to CCBs (OR, 0.96; 95% CI, 0.89–1.03; p = 0.24).

Conclusions: CCBs did not increase all-cause mortality incidence in patients with CKD though they displayed weaker renoprotective, compared to ACEIs or ARBs therapy. Our results suggest the combination of a CCB and an ACEI or ARB should be a preferable antihypertensive therapy in patients with CKD, considering their higher effect in decreasing blood pressure and fewer adverse metabolic problems caused.

september 22/2016

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Sodium and intravascular volumedietary sodium restriction and diuretic therapy may correct the increased water balance and prevent water retention from recurringadequate daily sodium intake in healthy children is only 1.2 g/day for four to eight year-old children and 1.5 g/day for older children / 2 to 3 g/day … in general/Diuretic therapy includes either loop diuretics such as furosemideSome children with obstructive uropathy and/or dysplastic kidneys have hypovolemia and hyponatremia. require ongoing fluid and sodium replacement

september 22/2016

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cont…..treatmenthyperkalemiaLow potassium diet. Administration of a loop diureticResin therapy. If failed do RRT

• Metabolic acidosis–maintain the serum bicarbonate level at or

above 22 mEq/L(sodium bicarbonate )

september 22/2016

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Cont..d• Bone deformity:-using both dietary and pharmacologic

interventions– low-phosphorus diet– so phosphate binders are used to enhance fecal phosphate excretion-- Vitamin D therapy is the corner stone therapy

• According to alberz et.al 2012. “oral cholecalciferol regimen was safe and sufficient to maintain serum 25(OH)D concentrations and prevent vitamin D insufficiency in early CKD. Furthermore, serum PTH improved after cholecalciferol treatment, particularly in patients who had secondary hyperparathyroidism”.

september 22/2016

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Treatment of Anemia

Recombinant human erythropoietin (rHuEPO)• hemoglobin concentration falls below

10 g/dL, at a dose of 50-150 mg/kg/dose subcutaneously 1-3 times weekly.

• All patients receiving rHuEPO therapy should be provided with either oral or intravenous iron supplementation(SusanM. Koshy & Denis F. Geary 2008).september 22/2016

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Nutrition

• Energy– based upon the estimated energy requirement (EER) for

chronological age • Protein – Should be 2.5 g/kg/24 hr and should consist of proteins of

high biologic value that are metabolized primarily to usable amino acids rather than to nitrogenous wastes.

– The proteins of highest biologic value are those of eggs and milk, followed by meat, fish, and fowl

• Vitamins and minerals– can become deficient in water-soluble vitamins either because

of inadequate dietary intake or dialysis lossesseptember 22/2016

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Growth

Treatment with rHuGH continues until the patient reaches the 50th percentile for

midparental height or achieves a final adult height or undergoes kidney transplantation

september 22/2016

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Immunization

• Children with CKD should receive all standard

immunizations according to the schedule used

for healthy children

• An exception must be made in withholding live

virus vaccines from children with CKD related to

glomerulonephritis, or any diseaseseptember 22/2016

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End-Stage Renal Disease

– The state in which a patient's renal dysfunction has progressed to

the point at which homeostasis and survival can no longer be

sustained with native kidney function and maximal medical

management.

– At this point, renal replacement therapy (dialysis or

renal transplantation) becomes necessary

– It is recommended that plans for renal replacement therapy be

initiated when a child reaches stage 4 CKDseptember 22/2016

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Survival patterns of patients on maintenance hemodialysis

Dialysis treatment Forty-one (45.1%) deaths occurred during dialysis treatment and 21 (23.1%) of patients died within the first 90 days of starting

dialysis. Only 42.1% of them survived longer than a year.

The frequently registered causes of death were septicemia (34.1%) and cardiovascular diseases (29.3%). Use of catheter as vascular access was associated with decreased short term and long term survival (Tamiru .et al.2013 ).

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Nursing Management1. Assessing fluid status and identifying potential sources of

imbalance.

2. implementing a dietary program to ensure proper nutritional intake

3. promoting positive feelings by encouraging increased self-care and greater independence.

4. Provide explanations and information to the patient and family concerning AKI, treatment options and potential complications.

5. Provide emotional support to the patient and family

6. prepare the child/family in whom renal replacement therapyseptember 22/2016

83

Reference 1. Scott M. Sutherland et.al. AKI in Hospitalized Children: Comparing the pRIFLE, AKIN, and KDIG Definitions Department of Pediatrics, Stanford University and Center for Acute Care Clin J Am Soc Nephrol 10: 554–561, April, 2015). 2015.2. Zappitelli et al. Association of Definition of Acute Kidney Injury by Cystatin C Rise With Biomarkers and Clinical Outcomes in Children Undergoing Cardiac Surgery JAMA Pediatr. 2015 June 1; 169(6).3. Paweena S.et.al, World Incidence of AKI: A Meta-Analysis Clin J Am Soc Nephrol. 2013 Sep 6; 8(9): 1482–1493.4. Jai Prakash1Changing epidemiology of community-acquired acute kidney injury in developing countries: analysis of 2405 cases in 26 years from eastern IndiaClin Kidney J (2013) 6: 150–155.5. Shimelis D, Tadesse Y. Department of Pediatrics and Child Health, Tikur Anbessa Hospital, Addis Ababa, Ethiopian medical journal 2004, 7-22.6. Alobaidi et al. Sepsis-Associated Acute Kidney InjurySemin Nephrol 2015 January ; 35(1): 2.7. Sarah Faubel et.al. Renal Relevant Radiology: Use of Ultrasonography in Patients with AKI,Clin J Am Soc Nephrol. 2014 Feb 7; 9(2): 382–394.8.ProwleJ et.al. Fluid management for the prevention and attenuation of acute kidney injury Nat. Rev. Nephrol. 2014, 10, 37–47 .9. Branza et.al.A comparison between fenoldopam and low-dose dopamine in early renal dysfunction of critically ill patients. Crit Care Med.2006;34:707–14.10..Wuhi E, Trivelli A,et.al.strict blood pressure control and progression of renal failure in children .N Engl J M ed 2009;361:1639.

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Cont…reference11. Fiaccadori E, Parenti E, Maggiore U. Nutritional support in acute kidney injury. J Nephrol.

2008;21:645–5612.KIDIGO 2012,Guideline13. Cynthia J.Wong. CKiD (CKD in Children) Prospective Cohort Study: Am J Kidney Dis 2012;60;6.)14.coca et.al. chronic kidney disease after acute kidney injury. epidemiological research center,2012.15 Hong-Jin Zhao. Effect of calcium channels blockers and inhibitors of the renin-angiotensin system

on renal outcomes and mortality in patients suffering from chronic kidney disease: systematic review and meta-analysis,2016.

16. Alvarez et.al. High-dose cholecalciferol reduces parathyroid hormone in patients with early chronic J Clin Nutr 2012;96:672–9.

17. Susan M. Koshy & Denis F. Geary .Anemia in children with chronic kidney disease, Pediatr Nephrol 200823:209–219)

18 Esposito S et.al .administration in children with chronic kidney disease,2014,20:32.19. Rajit K. Basu Acute Renal Replacement Therapy in Pediatrics, International Journal of

Nephrology ;2011,Volume 2011 20. Tamiru .et al. Survival patterns of patients on maintenance hemodialysis for end stage renal

disease in Ethiopia: BMC Nephrology 2013,14 :12721. Nelson textbook of pediatrics 20 ed,201522. Up to date 21.2

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THANKYOU

september 22/2016