Acute Kidney injury AKI................ppt

Life savings methods,and procedure

1. Seminar: Acute Kidney Injury in Children
Moderator: Dr. Girma (MD, Pediatrician, Ass.
Professor of Pediatrics & Child Health)
Presenter: Alehegn W. (C-1)
June, 2024
Yekatit 12 Hospital Medical College
School of Medicine
Department of Pediatrics & Child Health

2. Outline
An Overview of Kidney anatomy
Glomerular Filtration
Tubular Function
Acute Kidney Injury:
Definition
Classification
Pathogenesis
Clinical manifestations and diagnosis
Laboratory findings
Principles of treatment
Prognosis

3. Kidney anatomy
Lie in the retroperitoneal space slightly above the level
of the umbilicus.
Range in length and weight, respectively, from
approximately 6 cm and 24 g in a full-term newborn.
2 layers:
-Outercortex, which contains:
-glomeruli
-convoluted tubules, and
-collecting ducts
-Innermedulla, which contains:
straight portions of the tubules, the loops of Henle, the
vasa recta, and the terminal collecting ducts.

4. Kidney anatomy…
Each kidney contains approximately 1 million
nephrons (each consisting of a glomerulus and
associated tubules).
There is a large variationin distribution of normal
nephron numbers in humans, ranging from 200,000 to
1.8 million nephrons per kidney.

5. Kidney anatomy…Blood Supply
Usually consists of a main renal artery that arises from
the aorta.
The main artery divides into segmental branches within
the medulla, becoming the interlobar arteries that pass
through the medulla to the corticomedullary junction.
At this point, the interlobar arteries branch to form the
arcuate arteries, which run parallel to the surface of the
kidney.
Interlobular arteries originate from the arcuate arteries
and give rise to the afferent arterioles of the glomeruli.

6. Kidney anatomy…Blood
Supply

7. Kidney anatomy…Blood
Supply
The juxtaglomerular apparatus is formed by:
Specialized muscle cells in the wall of the afferent
arteriole
Specialized distal tubular cells adjacent to the
glomerulus (macula densa) that controls the secretion of
renin.
•The afferent arteriole divides into the glomerular
capillary network, which then recombines into the
efferent arteriole.
•The juxtamedullary efferent arterioles are larger than
those in the corticaland provide the blood supply, as the
vasa recta, to the tubules and medulla.

8. Anatomy Of Glomerulus

9. Glomerular Filtration
The glomerular network of specialized capillaries
serves as the filtering mechanism of the kidney.
Lined by endothelial cells and have very thin
cytoplasm that contains many holes (fenestrations).
The glomerular basement membrane (GBM)
forms a continuous layer between the endothelial
and mesangial cells on one side and the epithelial
cells on the other.

10. Glomerular Filtration…
The GBM has three layers: a central electron-
dense lamina densa; the lamina rara interna, which
lies between the lamina densa and the endothelial
cells; and the lamina rara externa, which lies
between the lamina densa and the epithelial cells.
Kidney function is best measured as (GFR).
eGFR = 0.413 x height (cm) / serum creatinine
(Scr in mg/dl)

11. Acute Kidney Injury
Defined as an abrupt loss of kidney function
leading to:
A rapid decline in the glomerular filtration rate
(GFR)
Accumulation of waste products such as blood
urea nitrogen (BUN) and creatinine, and
Dysregulation of extracellular volume and
electrolyte homeostasis.

12. Acute Kidney Injury…
•Embodies a continuum of renal dysfunction that
ranges from a small increase in serum creatinine
to complete anuric renal failure.
•Incidence varies from 5–10% of all
hospitalizations to >25% in critically ill infants
and children.

13. Acute Kidney Injury…
KDIGO defines as:
Increase in serum creatinine by ≥0.3 mg/dL from
baseline within 48 hours, or
Increase in serum creatinine to ≥1.5 times baseline
within the prior 7 days, or
Urine volume ≤0.5 mL/kg/hr for 6 hours

14. Acute Kidney Injury…

16. AKI … Pathogenesis
Has been conventionally classified into three
categories: prerenal, intrinsic renal, and
postrenal.
Prerenal AKI, aka prerenal azotemia,
characterized by :
Diminished effective circulating arterial volume,
which leads to inadequate kidney perfusion and a
decreased GFR.
Evidence of structural kidney damage is largely
absent.

17. AKI … Pathogenesis
Common causes of prerenal AKI include
dehydration, sepsis, hemorrhage, severe
hypoalbuminemia, and cardiac failure.
If the underlying cause of the kidney
hypoperfusionis reversed promptly, kidney
function returns to normal.

18. AKI … Pathogenesis

19. AKI … Pathogenesis
Intrinsic renal AKI:
A variety of disorders characterized by kidney
parenchymal damage, including sustained
hypoperfusion and ischemia.
Ischemic/hypoxic injury and nephrotoxic insults are
the most common causes.

20. AKI … Pathogenesis
More common with an underlying comorbid
condition; most are associated with cardiac,
oncologic, urologic, kidney, and genetic disorders
or prematurity.
Severe and prolonged ischemic/hypoxic injury
and nephrotoxic insult lead to acute
tubularnecrosis (ATN), seen most often in
critically ill infants and children.

21. AKI … Pathogenesis
Postrenal AKI:
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 most
cases.
In a patient with two functioning kidneys,
obstruction must be bilateral to result in AKI.

22. Clinical manifestations and diagnosis
A carefully taken history is critical in defining the
cause:
An infantwith a three day history of vomiting and
diarrhea most likely has prerenal AKI caused by
volume depletion, but hemolytic-uremic syndrome
(HUS) must also be a consideration.
A 6-year-old child with a recent pharyngitis who
presents with periorbital edema, hypertension, and
gross hematuria most likely has intrinsic injury
related to acute glomerulonephritis.

23. Clinical manifestations and diagnosis
A critically ill child with a history of protracted
hypotension or with exposure to nephrotoxic
medications most likely has ATN.
A neonatewith a history of hydronephrosis seen
on prenatal ultrasound studies and a palpable
bladder most likely has congenital urinary tract
obstruction, probably related to posterior urethral
valves.

24. Clinical manifestations and diagnosis
Thorough physical examination:
Careful attention to volume status.
Tachycardia, dry mucous membranes, and poor
peripheral perfusion suggest an inadequate circulating
volume.
Hypertension, peripheral edema, rales, and a cardiac
gallop suggest volume overload and the possibility of
intrinsic injury from glomerulonephritis or ATN.

25. Clinical manifestations and diagnosis
Rash and arthritis might indicate SLE or IgA
vasculitis nephritis.
Palpable flank masses may be seen with renal vein
thrombosis, tumors, cystic disease, or urinary tract
obstruction. 

26. Clinical manifestations and diagnosis
Laboratory findings:
Urinalysis-hematuria, proteinuria, and red
blood cell or granular urinary casts.
CBC-anemia (usually dilutional or hemolytic),
thrombocytopenia
•Hyponatremia (dilutional); metabolic acidosis
•Elevated serum concentrations of blood urea
nitrogen (BUN), creatinine, uric acid,
potassium, and phosphate (diminished kidney
function)

27. Clinical manifestations and diagnosis…
•Hypocalcemia (hyperphosphatemia).
•Urinary indices may be useful in differentiating
prerenal from intrinsic AKI.
•Urinary indices: prerenal versus intrinsic causes.

28. Clinical manifestations and diagnosis…
Chest radiography -reveals cardiomegaly,
pulmonary congestion (fluid overload), or pleural
effusions.
Renal ultrasonography -reveals hydronephrosis
and/or hydroureter, which suggest urinary tract
obstruction, or nephromegaly, consistent with
intrinsic renal disease.
Renal biopsy-to determine the precise cause.
Serum creatinine -an insensitive and
delayed measure.

29. Clinical manifestations and diagnosis

30. Principles of Treatment
IV volume expansion -administration of isotonic
saline, 20 mL/ kg over 30 minutes.
Catheterization-should be placed immediately to
ensure adequate drainage of the urinary tract.
Diuretic therapy -considered only after the
adequacy of the circulating blood volume has been
established.
Fluid restriction -If there is no response to a
diuretic challenge.
Nutrition

31. Principles of Treatment…
Managing complications:
-Hyperkalemia
-Mild metabolic acidosis
-Hypocalcemia
-Hyponatremia
-GI bleeding
-Hypertension
-Neurologic symptoms
-Anemia

32. Principles of Treatment…
Dialysis-Indications include:
-Anuria/oliguria with fluid overload
-Volume overload with evidence of hypertension
and/or pulmonary edema refractory to diuretic
therapy.
-Persistent hyperkalemia Severe metabolic acidosis
unresponsive to medical management
-Uremia (encephalopathy, pericarditis, neuropathy)
-Calcium: phosphorus imbalance, with hypocalcemic
tetany that can not be controlled by other measures.
-Inability to provide adequate nutritional intake
because of the need for severe fluid restriction.
Continuous renal replacement therapy (CRRT)

33. AKI Complications

34. Prognosis
Mortality rate in children is variable and depends
entirely on the nature of the underlying disease
process rather than on the renal failure itself.
Children with AKI caused by a kidney-limited
condition such as postinfectious
glomerulonephritis have a very low mortality rate
(<1%).
Those with AKI related to multiorgan failure have
a very high mortality rate (>50%).
Recovery of kidney function depends on the
disorder that precipitated AKI.

35. Prognosis…
Recovery is likely after AKI resulting from prerenal
causes, ATN, acute interstitial nephritis, or tumor
lysis syndrome.
Complete recovery of renal function is unusual from:
-Most types of rapidly progressive glomerulonephritis,
-Bilateral renal vein thrombosis
-Bilateral cortical necrosis.

36. References
Nelson Textbook of Pediatrics, 22nd Ed. 2024
Nelson Essentials of Pediatrics, 10
th
ed.
QuiZlet.com/Flashcards

37. I Thank
You!