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Disaster nephrology: a new concept for an old problem.

Sever MS, Lameire N, Van Biesen W, Vanholder R - Clin Kidney J (2015)

Bottom Line: However, despite the potentially negative impact on survival chances, these health care issues are often neglected by the authorities.Since many crush victims in spite of being rescued alive from under the rubble die afterward due to lack of dialysis possibilities, the terminology of 'renal disaster' was introduced after the Armenian earthquake.Learning and applying the basic principles of disaster nephrology is vital to minimize the risk of death both in AKI and CKD patients.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine/Nephrology , Istanbul School of Medicine , Istanbul , Turkey.

ABSTRACT
Natural and man-made mass disasters directly or indirectly affect huge populations, who need basic infrastructural help and support to survive. However, despite the potentially negative impact on survival chances, these health care issues are often neglected by the authorities. Treatment of both acute and chronic kidney diseases (CKDs) is especially problematic after disasters, because they almost always require complex technology and equipment, whereas specific drugs may be difficult to acquire for the treatment of the chronic kidney patients. Since many crush victims in spite of being rescued alive from under the rubble die afterward due to lack of dialysis possibilities, the terminology of 'renal disaster' was introduced after the Armenian earthquake. It should be remembered that apart from crush syndrome, multiple aetiologies of acute kidney injury (AKI) may be at play in disaster circumstances. The term 'seismonephrology' (or earthquake nephrology) was introduced to describe the need to treat not only a large number of AKI cases, but the management of patients with CKD not yet on renal replacement, as well as of patients on haemodialysis or peritoneal dialysis and transplanted patients. This wording was later replaced by 'disaster nephrology', because besides earthquakes, many other disasters such as hurricanes, tsunamis or wars may have a negative impact on the ultimate outcome of kidney patients. Disaster nephrology describes the handling of the many medical and logistic problems in treating kidney patients in difficult circumstances and also to avoid post-disaster chaos, which can be made possible by preparing medical and logistic scenarios. Learning and applying the basic principles of disaster nephrology is vital to minimize the risk of death both in AKI and CKD patients.

No MeSH data available.


Related in: MedlinePlus

Pathogenesis of AKI related to the crush syndrome. 1. Muscle necrosis causes dramatic fluid third spacing, leading to intravascular volume depletion, renal hypoperfusion and ischaemia. 2. Myoglobinuria causes intratubular cast formation, which contributes to AKI. 3. Scavenging of nitric oxide by myoglobin and activation of the inflammatory pathways due to severe muscle injury, can aggravate renal hypoperfusion and tissue injury. 4. Nucleosides released from disintegrating cell nuclei, and metabolized to uric acid, may contribute to cast formation and tubular obstruction. 5. Degradation of intratubular myoglobin causes release of free iron, which catalyses free radical production enhancing ischaemic damage. 6. Hyperkalaemia depresses cardiac output potentiating renal hypoperfusion. 7. Hyperphosphataemia may contribute to hypocalcaemia, which can further depress myocardial contractility, and may result in the precipitation of CaPO4 salts that induce inflammation of the kidney tissue. 8. Damaged muscles can release tissue thromboplastin, triggering disseminated intravascular coagulation (adapted from [44]). IVV: intravascular volume; ATN: acute tubular necrosis; AKI: acute kidney injury; DIC: disseminated intravascular coagulation; NO: nitric oxide.
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SFV024F2: Pathogenesis of AKI related to the crush syndrome. 1. Muscle necrosis causes dramatic fluid third spacing, leading to intravascular volume depletion, renal hypoperfusion and ischaemia. 2. Myoglobinuria causes intratubular cast formation, which contributes to AKI. 3. Scavenging of nitric oxide by myoglobin and activation of the inflammatory pathways due to severe muscle injury, can aggravate renal hypoperfusion and tissue injury. 4. Nucleosides released from disintegrating cell nuclei, and metabolized to uric acid, may contribute to cast formation and tubular obstruction. 5. Degradation of intratubular myoglobin causes release of free iron, which catalyses free radical production enhancing ischaemic damage. 6. Hyperkalaemia depresses cardiac output potentiating renal hypoperfusion. 7. Hyperphosphataemia may contribute to hypocalcaemia, which can further depress myocardial contractility, and may result in the precipitation of CaPO4 salts that induce inflammation of the kidney tissue. 8. Damaged muscles can release tissue thromboplastin, triggering disseminated intravascular coagulation (adapted from [44]). IVV: intravascular volume; ATN: acute tubular necrosis; AKI: acute kidney injury; DIC: disseminated intravascular coagulation; NO: nitric oxide.

Mentions: Also, the pathogenesis of crush syndrome-related AKI after rhabdomyolysis is multifactorial (Figure 2) [8, 43, 45–47]. The most important factor is hypovolaemia, leading to renal hypoperfusion and ischaemia, meaning that AKI at the beginning is often prerenal; however, if not treated properly, ATN develops. In addition, myoglobinuria, free radical production renal hypoperfusion due to the negative inotropic effect of hyperkalaemia and hypocalcaemia can play a role in the pathogenesis of AKI (Figure 2).Fig. 2.


Disaster nephrology: a new concept for an old problem.

Sever MS, Lameire N, Van Biesen W, Vanholder R - Clin Kidney J (2015)

Pathogenesis of AKI related to the crush syndrome. 1. Muscle necrosis causes dramatic fluid third spacing, leading to intravascular volume depletion, renal hypoperfusion and ischaemia. 2. Myoglobinuria causes intratubular cast formation, which contributes to AKI. 3. Scavenging of nitric oxide by myoglobin and activation of the inflammatory pathways due to severe muscle injury, can aggravate renal hypoperfusion and tissue injury. 4. Nucleosides released from disintegrating cell nuclei, and metabolized to uric acid, may contribute to cast formation and tubular obstruction. 5. Degradation of intratubular myoglobin causes release of free iron, which catalyses free radical production enhancing ischaemic damage. 6. Hyperkalaemia depresses cardiac output potentiating renal hypoperfusion. 7. Hyperphosphataemia may contribute to hypocalcaemia, which can further depress myocardial contractility, and may result in the precipitation of CaPO4 salts that induce inflammation of the kidney tissue. 8. Damaged muscles can release tissue thromboplastin, triggering disseminated intravascular coagulation (adapted from [44]). IVV: intravascular volume; ATN: acute tubular necrosis; AKI: acute kidney injury; DIC: disseminated intravascular coagulation; NO: nitric oxide.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4440471&req=5

SFV024F2: Pathogenesis of AKI related to the crush syndrome. 1. Muscle necrosis causes dramatic fluid third spacing, leading to intravascular volume depletion, renal hypoperfusion and ischaemia. 2. Myoglobinuria causes intratubular cast formation, which contributes to AKI. 3. Scavenging of nitric oxide by myoglobin and activation of the inflammatory pathways due to severe muscle injury, can aggravate renal hypoperfusion and tissue injury. 4. Nucleosides released from disintegrating cell nuclei, and metabolized to uric acid, may contribute to cast formation and tubular obstruction. 5. Degradation of intratubular myoglobin causes release of free iron, which catalyses free radical production enhancing ischaemic damage. 6. Hyperkalaemia depresses cardiac output potentiating renal hypoperfusion. 7. Hyperphosphataemia may contribute to hypocalcaemia, which can further depress myocardial contractility, and may result in the precipitation of CaPO4 salts that induce inflammation of the kidney tissue. 8. Damaged muscles can release tissue thromboplastin, triggering disseminated intravascular coagulation (adapted from [44]). IVV: intravascular volume; ATN: acute tubular necrosis; AKI: acute kidney injury; DIC: disseminated intravascular coagulation; NO: nitric oxide.
Mentions: Also, the pathogenesis of crush syndrome-related AKI after rhabdomyolysis is multifactorial (Figure 2) [8, 43, 45–47]. The most important factor is hypovolaemia, leading to renal hypoperfusion and ischaemia, meaning that AKI at the beginning is often prerenal; however, if not treated properly, ATN develops. In addition, myoglobinuria, free radical production renal hypoperfusion due to the negative inotropic effect of hyperkalaemia and hypocalcaemia can play a role in the pathogenesis of AKI (Figure 2).Fig. 2.

Bottom Line: However, despite the potentially negative impact on survival chances, these health care issues are often neglected by the authorities.Since many crush victims in spite of being rescued alive from under the rubble die afterward due to lack of dialysis possibilities, the terminology of 'renal disaster' was introduced after the Armenian earthquake.Learning and applying the basic principles of disaster nephrology is vital to minimize the risk of death both in AKI and CKD patients.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine/Nephrology , Istanbul School of Medicine , Istanbul , Turkey.

ABSTRACT
Natural and man-made mass disasters directly or indirectly affect huge populations, who need basic infrastructural help and support to survive. However, despite the potentially negative impact on survival chances, these health care issues are often neglected by the authorities. Treatment of both acute and chronic kidney diseases (CKDs) is especially problematic after disasters, because they almost always require complex technology and equipment, whereas specific drugs may be difficult to acquire for the treatment of the chronic kidney patients. Since many crush victims in spite of being rescued alive from under the rubble die afterward due to lack of dialysis possibilities, the terminology of 'renal disaster' was introduced after the Armenian earthquake. It should be remembered that apart from crush syndrome, multiple aetiologies of acute kidney injury (AKI) may be at play in disaster circumstances. The term 'seismonephrology' (or earthquake nephrology) was introduced to describe the need to treat not only a large number of AKI cases, but the management of patients with CKD not yet on renal replacement, as well as of patients on haemodialysis or peritoneal dialysis and transplanted patients. This wording was later replaced by 'disaster nephrology', because besides earthquakes, many other disasters such as hurricanes, tsunamis or wars may have a negative impact on the ultimate outcome of kidney patients. Disaster nephrology describes the handling of the many medical and logistic problems in treating kidney patients in difficult circumstances and also to avoid post-disaster chaos, which can be made possible by preparing medical and logistic scenarios. Learning and applying the basic principles of disaster nephrology is vital to minimize the risk of death both in AKI and CKD patients.

No MeSH data available.


Related in: MedlinePlus