Acute Tubular Necrosis

Acute parenchymatous renal failure (acute tubular necrosis, ATN, ARF) is direct damage to the renal parenchyma, most commonly ischemic' or toxic'. ATN is usually associated with oliguria (diuresis < 500 ml/day), and brownish cylinders tend to be present in Urinary Sediment Examination.

ATN can develop from prerenal failure on the basis of vasoconstriction with subsequent development of tubular necrosis, it can arise from hypoxic-ischemic damage, toxic damage' to tubular cells by drugs, contrast agents, exogenous and endogenous toxins.

Prognosis of ATN' is good, except for severe involvement with thrombus formation in the microcirculation with development of cortical necrosis. The mortality and morbidity of children with ARF is worse in neonates and children with multiorgan involvement. Renal function in children with ATN who recover normalizes. In some children renal function may take several days to recover, in others several weeks. The recovery of renal function may be accompanied by a polyuric phase, which is less common in children than in adults.

Etiopathogenesis

Ischemic ARS

A decrease in renal function due to ischemic tubular damage as a consequence of renal hypoperfusion (most commonly shock) is manifested:

1. decrease in blood flow (mainly through the cortex),
2. decrease in capillary wall permeability,
3. reflux of filtrate through the damaged tubule wall into the interstitium,
4. blockage of the tubules.

Prolonged ischaemia reduces production of vasodilator actions and stimulates production of vasoconstrictors → deepening of ischaemia → tubular necrosis. This allows the filtrate to reflux through the necrotic epithelium back into the interstitium, rendering filtration ineffective; moreover, sloughed tubular cells can occlude the tubule lumen → ↑ tubular pressure and stop glomerular filtration.

Nephrotoxic ARS (nephrotoxic damage or severe TIN) =

Nephrotoxic ARS can be caused by internal (endogenous) or external (exogenous) influences.

Exogenous influences include:

1. antibiotics - aminoglycosides depositing in the proximal tubule and ensuring release of lysosomes → destruction; sulfonamides causing tubule obstruction by crystals; tetracyclines and amphotericin B,
2. 'contrast agents',
3. 'heavy metals' (Hg, Pb, etc.),
4. 'chemotherapeutics - methotrexate; cisplatin - damages mitochondria, blocks ATPase; mitomycin
5. 'immunosuppressants - cyclosporine - intrarenal constriction of afferent arteriole,
6. 'organic solvents' - ethylene glycol.

The endogenous influences include:

Intratubular precipitation of hemoglobinu or myoglobinu - rhabdomyolysis: crush syndrome, ischemic muscle damage, ketoacidosis, infection, cocaine.

Laboratory findings

Excretion fraction of Na⁺ >3%, osmolarity approaches plasma.

Clinical picture and course

ARS persists after renal perfusion is restored; prerenal ARS may correct immediately. The course can be divided into three phases. The first is the initiation phase when insult occurs and oliguria can still be prevented. The second phase is the advanced ARS phase', when oliguria occurs, which lasts 7-14 days; in this phase there is a risk of: hyperhydration, ion imbalance (mainly hyperkalemia), acidosis, uremic syndrome. The last phase is the reparation phase, when function is gradually restored, tubular flow is restored; first diuresis → inability to concentrate - polyuric phase, when concentration impairment persists for many months.

Therapy

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Treatment of acute kidney failure takes place in the nephrology department / ICU. During treatment, it is important to ensure and monitor basic vital functions; fluid balancing with accurate urine collection and hydration status monitoring.

Postrenal ASL: recovery of urine drainage mechanically can take place naturally (urinary catheter, stent) or outside of natural pathways (percutaneous epicystostomy, puncture nephrostomy); then remove your own obstacle at the appropriate time.

Prerenal ASL: restoration of renal perfusion pressure → mean arterial pressure (MAP) 75–80 mm Hg: replenishment of circulating volume in true hypovolemia according to the nature of losses (electrolyte solutions , plasma, blood), improvement of the effective plasma volume in false hypovolemia (plasma expanders, albumin, plasma or blood); MAP < 70 mm Hg: volume adjustment + vasopressor drugs.

Other cases + renal ASL: treatment according to the cause.

Restoration of diuresis in oligoanuria:

• ensuring normovolemia – furosemide in a maximum dose of up to 500 mg i.v. within 30 min,
• 20% mannitol 100–250 ml for crush syndrome + myoglobinuria,
• continuous administration of dopamine at 1.5–2.5 μg/kg/min → vasodilation in the kidneys.

Hyperkalemia: restriction of potassium intake → in case of acute threat:

• acute hemodialysis (most effective),
• 10% calcium gluconicum 10–30 ml i.v. / NaCl 10–30 ml i.v. (inhibition of membrane effect K),
• 40% Glc 250 ml + 24 IU Ins / 8.4% NaHCO₃> 100 ml in 30 min infusion (support of K utilization in the cell),
• ion exchangers Resonium A / Calcium Resonium 1–2 scoops after 2–4 p.o. with lactulose / in a rectal enema.

Hypokalemia (threatened in the polyuric phase of ASL, the onset of anabolism and adjustment MAC): K supplementation (potassium chloride).

Therapeutic nutrition: daily energy intake 160–200 kJ/kg; proteins 0.8–1.2 g/kg, carbohydrates 6–8 g/kg, fats up to 1 g/kg.

Renal function is replaced by extracorporeal purification methods, including intermittent hemodialysis + hemodiafiltration / continuous hemofiltration + hemodiafiltration).

References

Related articles

• Acute renal failure - Acute renal failure (pediatrics)
• Treatment of acute renal failure
• Chronic kidney disease

Source

• ŠTEFÁNEK, Jiří. Medicína, nemoci, studium na 1. LF UK [online]. [cit. 22. 4. 2010]. <https://www.stefajir.cz/>.