Acute kidney failure

from Wikipedia, the free encyclopedia
Classification according to ICD-10
N17.9 Acute kidney failure, unspecified
N17.0 Acute kidney failure with tubular necrosis
N17.1 Acute kidney failure with acute cortical necrosis
N17.2 Acute kidney failure with marrow necrosis
O90.4 Postpartum acute kidney failure
ICD-10 online (WHO version 2019)

When acute renal failure ( ARF ), and uremia , acute renal failure or acute kidney injury ( English acute kidney injury , AKI ), is it a sudden onset within hours or days, in principle back formable deterioration of filtrativen kidney function. It may by prior normal renal function or in already chronically impaired renal function (ANV on the floor of chronic renal failure, Eng. Acute on chronic renal failure ) as well as part of an acute kidney disease ( English acute kidney disease / disorder , AKD ) occur. The glomerular filtration rate (GFR for short) is a measure of the severity of kidney failure .

Clinical picture

Renal insufficiency is a "deficient kidney function as a result of failure or destruction of the glomeruli or tubules" regardless of the existence of an underlying renal disease . The kidneys are almost always healthy in case of kidney failure ( kidney failure without kidney disease ). The opposite is kidney disease without renal insufficiency . A distinction is also made between acute kidney damage (AKI), subclinical AKI (sAKI), acute kidney disease (AKD) and chronic kidney disease (CKD).

The causes are divided into prerenal, renal and postrenal according to the location of the damage. The cause of damage in front of the kidney ( prerenal ) is primarily a reduced blood volume (hypovolemia, e.g. in the case of bleeding, lack of fluid or heart failure) or a blood pressure that is too low ( cardiorenal syndrome , shock , hepatorenal syndrome ). Cardiac output is a measure of this prerenal damage. Acute renal damage, d. H. in the kidney itself ( intrarenal ) occurring bilateral renal diseases , may be varied; they are rare. These include a. acute glomerulonephritis and tubulointerstitial kidney diseases , but also drug side effects ( X-ray contrast media ). Postrenal , the trigger lies behind the kidneys in the lower urinary tract . These causes are also rare; A frequent example is urinary retention with backlog of urine in the kidneys in the benign enlargement of the prostate .

The consequences are regulation problems of the fluid, electrolyte and acid-base balance as well as end products of protein metabolism (including urea ) and other urinary substances (including creatinine ) remaining in the organism. Subsequently, the azotemia can lead to a life-threatening state of poisoning, from uremia to coma uraemicum .

Depending on the cause, intensive medical treatment with early temporary dialysis may be necessary. Even if the prognosis for the restoration of kidney function ad integrum is good, acute kidney failure due to secondary diseases (e.g. pneumonia , sepsis , myocardial infarction , multiple trauma ) can lead to an often fatal multiple organ failure . The risk of developing into chronic renal failure requiring dialysis depends on the cause.

When in medicine from kidney failure is mentioned, is always by mutual kidney failure expected. A unilateral kidney failure in a healthy second kidney is not discussed in the following. Unilateral extrarenal kidney failure is impossible. And in the case of unilateral intrarenal kidney failure, clinically relevant renal insufficiency is always reliably prevented by the second healthy kidney (exception: diseased single kidney ). This is another reason why the distinction between kidney failure and kidney disease is very important. In cases of doubt, the GFR can be determined separately; then the patient's GFR is the sum (and not the mean ) of the GFR of his two individual kidneys.

In premature infants and newborn renal failure is physiologically . With a weight of 1 kg the GFR is 0.2 ml / min and with a weight of 2 kg only 0.5 ml / min. Full term babies have a GFR = 1.5 ml / min.

Definition and staging

The spectrum of acute kidney failure ranges from a minimal increase in serum creatinine to complete loss of kidney function.

In 2004, at an international consensus conference, the 30 different definitions of acute kidney failure that had existed until then were replaced by a uniform definition and staging, the RIFLE criteria. RIFLE is an acronym and stands for R isk - I njury - F ailure - L oss - E SRD (End Stage Renal Disease), translated roughly: Risk - Damage - Failure (of the kidneys) - Loss (of kidney function) - Terminal kidney failure.

In order to meet the broad spectrum of the disease, in 2007 the term, acute renal failure '( Acute Renal Failure , abbreviated ARF) in another consensus conference by the term, acute kidney injury' ( Acute Kidney Injury , abbreviated AKI) replaced, although most do there is no actual kidney disease. Definition and staging have been streamlined.

Definition of acute kidney damage by the Acute Kidney Injury Network (AKIN definition)
Abrupt (within 48 hours) decrease in kidney function, defined by
  • an absolute increase in serum creatinine by ≥ 0.3 mg / dl (≥ 26.4 µmol / l),
  • a percentage increase in serum creatinine of ≥ 50% (to 1.5 times the initial value) or
  • a reduction in urine excretion to <0.5 (ml / kg) / h over more than 6 hours.
Staging of acute kidney damage
RIFLE stage AKIN stage Serum creatinine Urine output
Risk 1 1.5 to 1.9 fold increase in creatinine (RIFLE / AKIN) or

Creatinine rise ≥ 0.3 mg / dl (≥ 26.4 µmol / l) (AKIN)

<0.5 ml / kg / h for 6 h
Injury 2 2- to 2.9-fold increase in creatinine <0.5 ml / kg / h for 12 h
Failure 3 ≥ 3-fold increase in creatinine or

Serum creatinine ≥ 4 mg / dl (≥ 354 µmol / l) with an acute increase ≥ 0.5 mg / dl (≥ 44 µmol / l)

<0.3 ml / kg / h for 24 h or

lack of urine output ( anuria ) for 12 h

Loess * Permanent kidney failure for> 4 weeks
ESRD * Permanent kidney failure for> 3 months
*) The RIFLE stages "Loss" and "ESRD" are no longer taken into account in the AKIN stage classification as late effects of acute kidney damage

The weaknesses of the new definition and staging are:

  • the relationship between the individual stages and clinically relevant endpoints such as mortality or the need for renal replacement therapy has so far not been sufficiently verified statistically,
  • the staging does not address the causes of the acute deterioration in renal function
  • and in particular does not differentiate between deterioration in kidney function due to reduced blood flow, a urinary outflow disorder or damage to the kidney tissue.

Classification according to etiology

The classification of the ANV is etiological , i.e. based on causes. However, the following seamless division into three groups is common, depending on whether the location of the cause is before (pre-), in (intra-) or after (post-) the kidneys ( Latin ren ; adjective renal ).

Prerenal ANV

Acute kidney failure with a prerenal cause (i.e. in front of the kidney) is by far the most common form (arithmetically in more than 92% of cases; according to Gerd Herold in 60%; according to Harrison in 40 to 80%; according to the MSD manual in 50 % up to 80% of cases; according to Ulrich Thomae in about 80%). It is also known as prerenal azotemia . Here the kidney weakness is not based on structural or histological changes in the kidney tissue. Rather, it is a renal insufficiency without kidney disease. The cause is an insufficient cardiac output with renal hypoperfusion . Renal perfusion and thus glomerular filtration , i.e. ultimately the performance of the podocytes , decrease.

Regardless of the acuity (acute or chronic) one also speaks of the extrarenal kidney syndrome according to Wilhelm Nonnenbruch , therefore posthumously of the Nonnenbruch syndrome , of functional kidney failure , of prerenal kidney failure or of extrarenal renal insufficiency . The word extrarenal refers to both prerenal and postrenal causes ("extrarenal origin"). In numerical terms, however, the postrenal causes are negligible; they fall (almost exclusively) in the field of urology and not in nephrology. Prerenal kidney failure is the reversible impairment of the filtrative kidney function as a result of insufficient kidney perfusion.

The cause of acute prerenal kidney failure is absolute or relative

If, like Ulrich Thomae does not count the Post Renal Syndrome on the causes of renal failure, the will Prärenalsyndrome the extra renal syndromes . As a result, Wilhelm Nonnenbruch, who first described it , did not mention the postrenal syndromes in his standard work . Kidney failure is often due to causes independent of the kidneys.

Intrarenal ANV

A sudden failure of the excretory (ie the filtrative ) kidney function, usually as a complication of a bilateral ( "double-sided" , bilateral ) basic renal disease as the cause of renal insufficiency, is rare. Renal diseases ( intrinsic kidney diseases , i.e. a severe and mostly very painful nephropathy with involvement of both kidneys) as the cause can be found in a maximum of 3% of cases, according to Ulrich Thomae in about 20%, according to Gerd Herold in 35% and according to The Merck Manual in 10 to 40 percent of the cases.

One medical dictionary even doubted the existence of intrarenal kidney failure. Quote: "The acute kidney failure is not due to a kidney disease."

One speaks also of acute intrinsic kidney failure and briefly of acute renal kidney failure or of (acute or chronic) intrarenal kidney failure in distinction to extrarenal kidney failure. In the following, it should be noted that tubular diseases ( " tubal insufficiency " ) have no direct influence on glomerular filtration . Therefore, the term acute tubular necrosis as a synonym for acute kidney failure in the narrower sense should be rejected.

Examples of acute intrarenal kidney failure are:

Post-renal ANV

Acute postrenal renal failure is also rare (less than 5% of cases, 5 to 10% according to the MSD Manual , 9%, "at most 10% of all hospitalized ANV cases ") and mostly reversible . Unilateral outflow obstacles cannot normally cause clinically relevant renal insufficiency as long as the other kidney prevents it. Because of this and because of completely different therapeutic consequences, Ulrich Thomae does not count "postrenal obstruction with anuria and consecutive kidney failure as acute kidney failure". In addition, all of these causes are usually very painful, so they often lead to quick, successful (mostly urological) therapy. For example, a one-sided stone-related urinary obstruction does not initially impair the glomerular filtration of the affected kidney; Unilateral anuria is caused by complete tubular reabsorption of the primary urine.

Such causes downstream of the kidneys through obstruction or compression of the lower urinary tract lead to drainage disorders up to the urinary obstruction . examples are

Epidemiology

Only a few studies exist on the epidemiology of acute and acute-on-chronic kidney failure. In a population-based study in Scotland , the annual incidence of acute kidney failure was 1,811 cases per million people and the incidence of acute-on-chronic kidney failure was 336 cases per million people. The median age of patients with acute kidney failure was 76 years, and patients with acute-on-chronic kidney failure 80.5 years. The RIFLE classification allowed a prognosis for complete reversibility of renal failure, the need for renal replacement therapy , length of hospital stay and hospital mortality , but did not allow any prediction of mortality after 3 or 6 months.

Pathophysiology and pathogenesis

overview

The main trigger of acute kidney failure is an inadequate supply of oxygen to kidney tissue (e.g. due to insufficient blood flow), which leads to the destruction ( endothelial damage ) of functional cells.

The primary damage affects the tubular cells. When damaged , these highly active cells form highly viscous mucoprotein cylinders that clog the lumen of the tubules (English: cast = clogging, discharge). This obstruction is blamed for the failure of kidney function. It should not be forgotten, however, that the glomeruli and the tubules have completely different tasks and work largely separately and independently of each other. In each individual case, it must be explained how tubular damage leads to a reduction in GFR and, in particular, a possible oliguria or anuria. Corresponding evidence in histology is only rarely possible. Because tubulopathies (for example inflammation of the kidney tubules up to tubular necrosis ) cause (regardless of the GFR) a polyuria due to a reduced rate of reabsorption . This is probably one of the reasons why the term tubular necrosis is abandoned in the current specialist literature ("rendering the previously popular term acute tubular necrosis an inadequate description"); tubuloglomerular feedback is also no longer mentioned.

Only when the tubules are completely clogged by Ausgusszylinder, it is in fact the reverse failure with anuria in the affected nephron. Only then do the respective single nephron glomerular filtration rates (snGFR) decrease to 0 ml / min and the individual reabsorption rates to 0%. There is only speculation about the number of affected nephrons and about the reversibility of this flow obstruction by cell cylinders in the individual tubulopathies.

These speculations go back to the Danish physiologist Poul Kristian Brandt Rehberg. Building on his work from the 1920s, tubuloglomerular feedback and tubuloglomerular balance were further developed. Originally this now abandoned, but sometimes still learned, hypothesis goes back to Homer William Smith ( glomerulo-tubular balance ). Thereafter, the decrease in GFR up to the glomerular shutdown is caused by the decrease in the tubular reabsorption rate. The neurohumoral regulation of the (in wide areas) opposing development (tending to be reciprocal proportionality ) of the two parameters primary urination and secondary urination or the proportionality of glomerular filtration and tubular resorption are overlooked. The purpose of this autonomous regulation is to avoid unnecessary water loss, especially during high physical exertion with a corresponding increase in CO and GFR. In the average adult with acute kidney failure, a decrease in the tubular resorption rate by, for example, 10% with an induced decrease in the GFR also by 10% (according to the now obsolete feedback theory ) only insignificantly reduces the GFR from 150 l / d to 135 l / d, but the daily amount of urine increases from 1.5 l / d (= 1% of 150 l / d) to 13.5 l / d (= 10% of now 135 l / d ). That would be an extreme polyuria (compensatory "forced polyuria") and thus exactly the opposite of the postulated oliguria. The specialist literature even reports a polyuria of 70 l / d after successful treatment of acute postrenal kidney failure. The authors Klaus Thurau and John W. Boylan call for "further research"; they are currently calling their theory about the failure of the feedback mechanism of the juxtaglomerular apparatus "speculative". According to this theory, halving the tubular re-absorption function would reduce urine production to 60 ml / min [sic!] (= 86.4 l / d ). enlarge.

Causes of Acute Intrarenal Renal Failure

Basically, three cause complexes are described for the rare acute intrarenal kidney failure :

  • exogenous or endogenous vasoconstriction ( vasoconstriction )
  • Oxygen deficiency in the narrower sense ( hypoxia , ischemia )
  • Substances that are toxic to the kidneys (exogenous kidney toxins and endogenous nephrotoxins )

Vasoconstriction

For normal kidney function, an adequate blood supply via the afferent vessels ( vas afferens ) is important. Only in this way is a certain pressure available (filtration pressure), which ensures sufficient filtration of primary urine in the glomeruli ( see kidney ). Since the kidneys have a pronounced autoregulatory mechanism ( renin-angiotensin-aldosterone system ), systemic blood pressures of 80 mmHg are sufficient for normal filtration.

The stress reaction, especially in the form of the release of endogenous catecholamines, is also responsible for the loss of function of the kidneys in circulatory failure. If the systemic blood pressure falls below a limit value, the sympathetic counter-regulation through the action of these catecholamines on the afferent vas causes a further loss of perfusion. This also reduces the filtration pressure. A decrease in the filtration pressure by 10–15 mmHg can lead to a halt in filtration and thus to anuria [2].

In addition to the endogenous catecholamines, some cytokines released in sepsis and MODS also have a vasoconstrictive effect on the kidney vessels. They have a nephrotoxic effect (see also below under nephrotoxins ).

Hypoxia and ischemia

Hypoxia is defined as a lack of oxygen, and ischemia as insufficient blood flow to a tissue or organ. The cause can be insufficient oxygen uptake by the organism or the vasoconstriction mentioned above.

The result is a decrease in the energy carrier ATP in the cells as soon as the kidney cells fail to switch from aerobic to anaerobic glycolysis. Tubular cells only have this possibility to an extremely limited extent, which is the reason for their premature failure of function.

An ischemia duration of 25 minutes leads to minor morphological changes that can be reversed at any time. Even changes after 40–60 min of ischemia are still reversible. Only an oxygen deficit of two or more hours causes permanent changes in the structure and function of the kidney. [2]

Nephrotoxins

There are a number of different endogenous and exogenous substances that can be nephrotoxic.

On the endogenous side, the proteins hemoglobin and myoglobin released after massive hemolysis and muscle cell death are essential because they act directly on the tubular cells. The mediators released in the context of MODS or sepsis have a more indirect nephrotoxic effect via vasoconstriction (see above).

Among the numerous exogenous nephrotoxins playing aminoglycoside - antibiotics (such as gentamicin ) an important role, which is why their use in kidney-threatening situations (shock, renal disease) must be adjusted. Antibiotics against pancreatitis and MRSA infections have also shown strong negative effects on the patient's condition: within a very short time (2–3 hours) acute kidney failure occurred almost to the point of collapse due to multiple organ failure. Only immediate dialysis saved the patient. Another example of nephrotoxins are contrast media containing iodine. In the case of impaired kidney function, their use must be weighed up in each individual case.

Risk factors for acute kidney failure

Among the risk factors features are set, the probability increases of the occurrence of ARF:

  • Acute risk factors : volume deficiency, pronounced hypotension (drop in blood pressure), infection, hemolysis (release of hemoglobin, see above), rhabdomyolysis (muscle breakdown), acute pancreatitis , intravascular coagulation, therapy with nephrotoxic drugs

In the complex clinical pictures, multiple and multiple trauma , sepsis , pancreatitis and burns play a major role. If the kidney is not already affected, then multi-organ failure (MOV, MODS) represents a very high risk constellation for ANV.

Phasing of acute kidney failure

There are four classic phases in the ANV:

  1. Induction : occurrence of the damaging event with a decrease in renal blood flow and glomerular filtration and with tubular damage. No symptoms occur at this stage.
  2. Conservation : The conservation phase is characterized by oliguria. The diagnostic laboratory findings mentioned below are collected here. The duration ranges from days to weeks.
  3. Recovery : This phase is polyuric and usually lasts only days.
  4. Restitution : In 80–90% of patients there is a complete recovery of kidney function over the course of months. In the remaining patients, secondary conditions in the form of chronic kidney failure are to be expected.

This classic process is rarely observed in modern intensive care medicine, as pre-existing kidney diseases and multiple organ failure strongly modify the process.

diagnosis

anamnese

When collecting the medical history, according to the above-mentioned Risk factors are sought.

Status present

When assessing the status, it is necessary to look for signs of overhydration or dehydration . In addition, is palpation of the kidneys, bladder and prostate important.

Clinically, in emergency situations, hyperventilation , a foetor uraemicus and drowsiness up to coma uraemicum are noticeable.

Technical findings

The amount of urine per unit of time is easy to determine:

Anuria <50-100 ml / 24h
Oliguria <500 ml / 24h or <20 ml / h
Polyuria > 3000 ml / 24h or> 125 ml / h

Acute kidney failure can be an-, oligo- or polyuric. In order to estimate the excretion capacity of the kidneys, the so-called retention values ​​are used, which are the concentrations of urea and creatinine in the serum. These substances, which are the end products of protein metabolism, are not themselves toxic. Although urea disrupts the metabolism of the cell, it is not the cause of uremic syndrome. Other degradation products are toxic, the concentrations of which correlate with urea. Their retention leads to uremia , which means that elimination is imperative. These breakdown products can be removed from the organism using technical kidney replacement processes (dialysis, hemofiltration).

Urea (HSt) if the value is> 25–33 mmol / l (> 150–200 mg / dl) in olig- / anuria or> 50 mmol / l (> 300 mg / dl) in polyuria, then acute kidney failure is confirmed and a kidney replacement procedure is required indicated (hemofiltration, hemodialysis).
Creatinine (crea) Daily creatinine increase of> 0.5–2 mg / dl is a sign of kidney failure. Parameter is considered unsafe. Creatinine clearance (= GFR ) is better . whose drop to below 5 ml / min indicates the indication for a kidney replacement procedure.

The differential diagnosis between prerenal and intrarenal kidney failure is important:

Prerenal ANV Intrarenal ANV
Urine osmolality (mosmol) > 500 <300
Urine / plasma osmolality > 1.1 0.9-1.05
Urine sodium (mmol / l) <10 > 30-40
FE Na (%) <1 > 1

The fractional sodium excretion (FE Na ) is calculated as follows:

Differential diagnosis

If a leak occurs in the area of ​​the urinary tract with urine escaping into the abdominal cavity (for example as a result of a rupture of the bladder ), the urinary substances are absorbed back into the blood (reabsorption). Despite normal kidney function, urea and creatinine increase. This condition is known as pseudo-kidney failure.

therapy

If ANV has occurred, there is currently no form of therapy that could effectively interrupt the course. A distinction is made depending on the stage of the disease

  • preventive therapy and
  • Therapy for an outbreak of ANV.

Preventive Therapy

The goal is to restore adequate blood flow to the kidneys with adequate oxygenation to the kidney tissue as quickly as possible. If this succeeds, the kidneys show a good tendency to resume their function, otherwise there is a risk of manifest kidney failure.

Acute therapy is based on three pillars:

  1. Ensuring adequate kidney blood flow through volume substitution,
    if necessary under control of the central venous pressure (CVP)
  2. Ensuring a stable circulation , if necessary with the help of catecholamines ( dobutamine , noradrenaline )
  3. Experiment with loop or osmodiuretic

A special form is the contrast medium-induced kidney failure caused by X-ray contrast media . Since the time of administration of the contrast medium can usually be planned in advance, prophylaxis is possible for high-risk patients before the kidney damage occurs.

Renal blood flow

The danger of volume substitution lies in the volume overload of the circulation with the result of overhydration of the lungs ( pulmonary edema , fluid development ). The CVP should be set to 12 mmHg, the PCWP to values ​​of 15 mmHg. Depending on the electrolyte status, etc., crystalloid solutions are preferred.

Circulatory stabilization

Dobutamine is currently considered the most kidney-friendly catecholamine . Norepinephrine is recommended elsewhere [2].

The administration of dopamine in so-called kidney doses is currently rejected because the cardiac side effects, on the one hand, and the lack of prognostic advantages, on the other, tend to suggest disadvantages of this agent. Various studies showed no benefit in terms of outcome, increase in creatinine, number of dialysis patients or length of intensive care stay. In contrast, however, impairment through potential side effects is postulated.

Diuretics

Diuretics (here loop diuretics ) are drugs that can damage the kidneys; they deliberately worsen the reabsorption rate of the renal tubules . In addition, although the use of these agents can increase the diuresis , the prognosis of the ANV is not improved. The benefit of diuretics lies solely in the improved balancing option, i.e. in being able to control the water balance over a certain period of time.

In the case of postrenal kidney failure and anuria, this therapeutic approach is strictly contraindicated (i.e. to be rejected).

treatment

In contrast to the brain and heart, the loss of function in the kidney after an ischemic episode with cell death can often heal. The point of therapy in the case of an outbreak of ANV is to replace the kidney function with dialysis until the kidney functions again. Often, however, kidney function can be permanently improved by normalizing cardiac output even without kidney dialysis.

A renal replacement procedure is indicated in the case of otherwise uncontrollable overhydration, especially of the lungs, with a high serum potassium of over 6.5 mmol / l, with pronounced acidosis and with symptoms of uremia .

Hemofiltration , dialysis

In addition to stabilizing the circulation, these procedures are also used to improve blood flow to the kidneys. They are technically so simplified that they belong to the basic therapeutic repertoire of interdisciplinary intensive care medicine .

Treatment for postrenal causes

Basically, here the elimination of problems with drainage by a is urologist , either causally or by the contribution of stents (so-called because of their pigtail-like shape double-J catheter, DJ-ureteral stent ; English double pigtail stent ) to ensure in both ureters to the urine flow. In severe cases, a transurethral (also known as self catheterization ) or suprapubic urinary catheter , a urostoma or even a neobladder should be considered. Bilateral percutaneous nephrostomies are only required in very rare cases . In addition, the above. nephrological and intensive care principles.

forecast

Renal function recovery is often incomplete after acute kidney failure. For example, people who have already required dialysis treatment due to acute kidney failure have a significantly increased risk of developing progressive chronic kidney failure in the further course .

See also

literature

  • J. Eckart, H. Forst, H. Burchardi: Intensive Care Medicine - Compendium and revision course for interdisciplinary further education. 9th edition. ecomed, Munich 2004, ISBN 3-609-20177-0 .
  • Cord Schneuzer: Kidney. In: Jörg Braun, Roland Preuss (Ed.): Clinic Guide Intensive Care Medicine. 9th edition. Elsevier, Munich 2016, ISBN 978-3-437-23763-8 , pp. 401-414, here: pp. 402-407 ( acute kidney failure ).
  • Raphael Weiss, Melanie Meersch u. a .: Acute kidney damage. An often underestimated problem in perioperative medicine. In: Deutsches Ärzteblatt. Volume 116, Issue 49, December 6, 2019, pp. 833–841.

Web links

Individual evidence

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  2. ↑ Maxim Zetkin, Herbert Schaldach: Dictionary of Medicine. 1st edition. Verlag Volk und Gesundheit , Berlin 1956, p. 622. Identical up to the 4th edition, Berlin 1969. Not so clear from the 5th edition, Deutscher Taschenbuch Verlag , Munich 1974, ISBN 3-423-03029-1 .
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  5. ↑ In the Federal Supply Act , the "kidney damage without renal impairment" are mentioned in the appendix to § 2nd
  6. ↑ Raphael Weiss et al. a .: Acute kidney damage. An often underestimated problem in perioperative medicine. 2019, p. 835.
  7. ↑ Walter Siegenthaler (Ed.): Differential diagnosis of inner diseases. 15th edition. Georg Thieme Verlag , Stuttgart / New York 1984, ISBN 3-13-344815-3 , pp. 25.34 to 25.39.
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  41. ^ Joachim Girndt: Kidney and hypertension diseases in diabetics. Edition Medicine, Weinheim 1988, ISBN 3-527-15367-5 , p. 15.
  42. ↑ Jürgen Sökeland: Urology. 10th edition. Georg Thieme Verlag, Stuttgart / New York 1987, ISBN 3-13-300610-X , p. 28.
  43. ↑ Note: Even the existence of tubular diseases is controversial; No scientific work on this keyword can be found in the Google search. There are 26,700 hits for the keyword tubulopathy . Probably only a few of these studies show a direct and causal connection between histologically detectable damage to the renal tubules and the tubular reabsorption rate.
  44. ^ Franz Volhard : Before the therapy, the gods put the diagnosis , Hoffmann-La Roche , Grenzach 1952, p. 16.
  45. ↑ Hans Eduard Franz, Walter H. Hörl (Ed.): Blood purification process. 5th edition. Georg Thieme Verlag, Stuttgart / New York 1997, ISBN 3-13-497705-2 , p. 520.
  46. ↑ Rudolf Gross , Paul Schölmerich : 1000 memoranda of internal medicine. 2nd Edition. Schattauer Verlag , Stuttgart / New York 1978, ISBN 3-7945-0511-5 , p. 159, number 759.
  47. ↑ JS Christo, AM Rodrigues et al: Nitric oxide (NO) is associated with gentamicin (GENTA) nephrotoxicity and the renal function recovery after suspension of GENTA treatment in rats. In: Nitric oxide: biology and chemistry / official journal of the Nitric Oxide Society. Volume 24, number 2, March 2011, pp. 77-83, doi: 10.1016 / j.niox.2010.12.001 . PMID 21167952 .
  48. ↑ T. Ichimura, CC Hung et al: Kidney injury molecule-1: a tissue and urinary biomarker for nephrotoxicant-induced renal injury. In: American Journal of Physiology-Renal Physiology . Volume 286, No. 3, 2004, pp. F552-F563, doi: 10.1152 / ajprenal.00285.2002 . PMID 14600030 .
  49. ^ RA Goyer: Mechanisms of lead and cadmium nephrotoxicity. In: Toxicology Letters . Volume 46, Numbers 1-3, March 1989, pp. 153-162. PMID 2650022 . (Review).
  50. ↑ A. Stacchiotti, E. Borsani et al: Dose-dependent mercuric chloride tubular injury in rat kidney. In: Ultrastructural pathology. Volume 27, Number 4, 2003 Jul-Aug, pp. 253-259. PMID 12907370 .
  51. ↑ Dieter Klaus (Ed.): Nephrological diseases. (= General Practice Practice. Volume 7). Urban & Schwarzenberg , Munich / Vienna / Baltimore 1983, ISBN 3-541-10811-8 , p. 133.
  52. ↑ Dieter Klaus (Ed.): Nephrological diseases. (= General Practice Practice. Volume 7). Urban & Schwarzenberg, Munich / Vienna / Baltimore 1983, ISBN 3-541-10811-8 , p. 17.
  53. ↑ Harrison's Internal Medicine. 18th edition. McGraw-Hill, Berlin 2012, ISBN 978-3-940615-20-6 , p. 361.
  54. ↑ Gerd Harald Herold : Internal Medicine. Cologne 2019, ISBN 978-3-9814660-8-9 , p. 636.
  55. ↑ The MSD Manual. 6th edition. Urban & Fischer , Munich, Jena 2000, ISBN 3-437-21750-X , p. 2235.
  56. ↑ Dieter Klaus (Ed.): Nephrological diseases. (= General Practice Practice. Volume 7). Urban & Schwarzenberg , Munich / Vienna / Baltimore 1983, ISBN 3-541-10811-8 , p. 17; analogously also in Volume 18 ("Urological Diseases"), ISBN 3-541-13121-7 , p. 18.
  57. ↑ Nephrology. 6th edition. Georg Thieme Verlag, Stuttgart / New York 2015, ISBN 978-3-13-700206-2 , p. 488 (in the original the highest instead of the highest ).
  58. ^ Mark Dominik Alscher, Christiane Erley, Martin K. Kuhlmann: Nosocomiales acute kidney failure. In: Deutsches Ärzteblatt International. Volume 116, Issue A, Issue 9, March 1, 2019, pp. 149–158.
  59. ↑ Nephrology. 6th edition. Georg Thieme Verlag, Stuttgart / New York 2015, ISBN 978-3-13-700206-2 , p. 488.
  60. ^ Ulrich Thomae: Renal Insufficiency. Hoechst Aktiengesellschaft, Munich 1989, p. 19.
  61. ↑ Jörg Dötsch, Lutz T. Weber (ed.): Kidney diseases in childhood and adolescence. Springer-Verlag, Berlin 2017, ISBN 978-3-662-48788-4 , p. 172.
  62. ^ Hans-Hellmut Neumeyer: Acute kidney failure. In: blood purification procedures. 5th edition. Georg Thieme Verlag, Stuttgart / New York 1997, ISBN 3-13-497705-2 , p. 520.
  63. ↑ Helmut Geiger: Acute kidney failure. In: Helmut Geiger, Dietger Jonas, Tomas Lenz, Wolfgang Kramer (eds.): Kidney diseases. Schattauer , Stuttgart / New York 2003, ISBN 3-7945-2177-3 , p. 3.
  64. ^ Hans Joachim Sarre : Kidney Diseases , 4th Edition, Georg Thieme Verlag, Stuttgart 1976, ISBN 3-13-392804-X , p. 427.
  65. ↑ Walter Siegenthaler et al. (Ed.): Textbook of internal medicine. 3. Edition. Georg Thieme Verlag, Stuttgart / New York 1992, ISBN 3-13-624303-X , p. 524.
  66. ↑ Karl Schärer, Otto Mehls (Ed.): Pediatrische Nephrologie. Springer-Verlag , Berlin / Heidelberg 2002, ISBN 3-642-62621-1 , p. 77.
  67. ^ The Merck Manual. 20th edition. Kenilworth 2018, ISBN 978-0-911910-42-1 , p. 2076.
  68. ↑ Tariq Ali et al .: Incidence and Outcomes in Acute Kidney Injury: A Comprehensive Population-Based Study . In: J Am Soc Nephrol . No. 18 , 2007, p. 1292-1298 ( asnjournals.org ).
  69. ^ Klaus Thurau, John W. Boylan: Acute Renal Success - The Unexpected Logic of Oliguria in Acute Renal Failure. In: The American Journal of Medicine . Volume 61, September 1976, pp. 308-315.
  70. ↑ Helmut Geiger: Acute kidney failure. In: Helmut Geiger, Dietger Jonas, Tomas Lenz, Wolfgang Kramer (eds.): Kidney diseases. Schattauer, Stuttgart / New York 2003, ISBN 3-7945-2177-3 , p. 1.
  71. ^ The Merck Manual. 20th edition. Kenilworth 2018, ISBN 978-0-911910-42-1 , p. 2076.
  72. ↑ Nephrology. 6th edition. Georg Thieme Verlag, Stuttgart / New York 2015, ISBN 978-3-13-700206-2 , p. 476.
  73. ^ Karl Julius Ullrich , Klaus Hierholzer : Normal and pathological functions of the renal tubule , Verlag Hans Huber , Bern / Stuttgart 1965, DNB 458762938 .
  74. ↑ The SNGFR is normally 20–40 nl / min in humans and 20–40 µl / min in dogs. Source: Hans Joachim Sarre : Kidney Diseases , 4th edition, Georg Thieme Verlag, Stuttgart 1976, ISBN 3-13-392804-X , p. 12. Apparently, Sarre made a mistake here. Apparently he chose the wrong kidney function unit in the dog. Presumably he also means nanoliters and not microliters per minute.
  75. ↑ Poul Brandt Rehberg: About the determination of the amount of glomerular filtrate using creatinine as a kidney function test, along with some theories about urine preparation. In: Central sheet for internal medicine . Volume 50, 1929, pp. 367-377.
  76. ↑ Gerd Harald Herold : Internal Medicine. Self-published , Cologne 2019, ISBN 978-3-9814660-8-9 , p. 636.
  77. ^ Heinrich Holzgreve, Hans Bräuer: kidney, hypertension and edema. Picture atlas. Röhm Pharma , Weiterstadt without year, p. 65.
  78. ↑ Gert Mayer: The cardiorenal syndrome. Uni-Med-Verlag, Bremen / London / Boston 2013, ISBN 978-3-8374-1335-9 , p. 26.
  79. ↑ John W. Boylan, Peter Deetjen, Kurt Kramer : Kidney and water balance. Urban & Schwarzenberg, Munich / Berlin / Vienna 1970, ISBN 3-541-04911-1 , p. 32.
  80. ^ Klaus Thurau, John W. Boylan: Acute Renal Success - The Unexpected Logic of Oliguria in Acute Renal Failure. In: The American Journal of Medicine. Volume 61, September 1976, p. 313. On page 314, complete kidney failure is even referred to as bankruptcy .
  81. ^ J. Schnermann, FS Wright, JM Davis, W. von Stackelberg, G. Gill: Regulation of superficial nephron filtration rate by tubulo-glomerular feedback. In: Pflüger's archive . Issue 318, June 1970, pp. 147-175.
  82. ^ Heinrich Holzgreve, Hans Bräuer: kidney, hypertension and edema. Picture atlas. Röhm Pharma, Weiterstadt without year, p. 43.
  83. ↑ Hans Erhard Bock , KH Hildebrand, Hans Joachim Sarre (ed.): Franz Volhard : Recollections , Schattauer Verlag , Stuttgart, New York 1982, ISBN 3-7845-0898-X , p. 30.
  84. ^ Franz Volhard : Before the therapy, the gods put the diagnosis , Hoffmann-La Roche , Grenzach 1952, p. 9.
  85. ↑ Georg Sabin: The cardiogenic shock. Verlag W. Kohlhammer , Stuttgart / Berlin / Cologne / Mainz 1984, ISBN 3-17-008618-9 , p. 21.
  86. ↑ Marlys H. Witte, Floyd A. Short, Walter Hollander: Massive polyuria and natriuresis Following relief of urinary tract obstruction. In: The American Journal of Medicine. Volume 37, Issue 2, August 1964, pp. 320–326.
  87. ^ Klaus Thurau, John W. Boylan: Acute Renal Success - The Unexpected Logic of Oliguria in Acute Renal Failure. In: The American Journal of Medicine. Volume 61, September 1976, p. 314.
  88. ^ Klaus Thurau, John W. Boylan: Acute Renal Success - The Unexpected Logic of Oliguria in Acute Renal Failure. In: The American Journal of Medicine. Volume 61, September 1976, p. 311.
  89. ↑ This research won the Nobel Prize in Physiology or Medicine in 2019 .
  90. ↑ R. Bellomo include: Lowdose dopamine in patients with early renal dysfunction: a placebo-controlled randomized trial. Australian and New Zealand Intensive Care Society (ANZICS) clinical trials group. In: The Lancet . Volume 356, 2000, pp. 2139-2143.
  91. ↑ Another view: Rudolf Gross , Paul Schölmerich : 1000 memoranda of internal medicine. 2nd Edition. Schattauer Verlag, Stuttgart / New York 1978, ISBN 3-7945-0511-5 , p. 158, number 759: "Acute kidney failure cannot be broken through by taking fluids alone! This only leads to overhydration." - This does not always apply if the acute kidney failure is based on an absolute or a relative volume deficiency (see above under the frequent prerenal causes).
  92. ↑ Cord Schneuzer: Kidney. In: Jörg Braun, Roland Preuss (Ed.): Clinic Guide Intensive Care Medicine. 9th edition. Urban & Schwarzenberg , Munich 2016, ISBN 978-3-437-23763-8 , p. 406 ( absolute indications for renal replacement therapy in ANV ).
  93. ^ Ron Wald et al: Chronic dialysis and death among survivors of acute kidney injury requiring dialysis . In: The Journal of the American Medical Association . tape 302 , no. 11 , September 16, 2009, p. 1179-1185 , doi : 10.1001 / jama.2009.1322 , PMID 19755696 .
  94. ↑ Lowell J. Lo et al .: Dialysis-requiring acute renal failure increases the risk of progressive chronic kidney disease . In: Kidney International . tape 76 , no. 8 , October 2009, p. 893-899 , doi : 10.1038 / ki.2009.289 , PMID 19641480 .
  95. ↑ Areef Ishani include: Acute kidney injury Increases risk of ESRD among elderly . In: Journal of the American Society of Nephrology . tape 20 , no. 1 , January 2009, p. 223-228 , doi : 10.1681 / ASN.2007080837 , PMID 19020007 .