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Nefrologi > Kronisk nyresykdom - Amboss > Flashcards

Kronisk nyresykdom - Amboss Flashcards

1
Q

Hvordan er prevalensen av kronisk nyresvikt?

Data fra USA

A
ESDR; End-stage renal disease. A terminal stage of renal failure characterized by a glomerular filtration rate (GFR) < 15 mL/min/1.73 m^2, requiring renal replacement therapy.
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2
Q

Hvordan er insidensen av KNS?

Data fra USA

A
In 2016, approx. 125,000 individuals started initial treatment for ESRD.
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3
Q

Hvilke risikofaktorer finnes for å utvikle KNS?

A
African American descent; This is partially due to APOL1, an autosomal recessive mutation, which is found exclusively in people with recent Sub-Saharan African ancestry.
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4
Q

Hvilken etiologi har KNS?

A

Amerikansk data

I Norge er det hypertensiv etiologi som oftest gir KNS.
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5
Q

Hva er patofysiologien til KNS avhengig av?

A
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6
Q

Hvordan er patofysiologien ved diabetisk nefropati?

A
GBM; Glomerular basement membrane. ECM; Extracellular matrix. TBM; Tubular basement membrane.
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7
Q

Hva er den underliggende patofysiologien ved hypertensiv nefropati?

A
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8
Q

Hva er patofysologien ved glomerulonefritt?

A
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9
Q

Hva er konsekvensene ved KNS?

A

Redusert GFR

Redusert endokrin aktivitet

Redusert glukoneogenese

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10
Q

Hva vil redusert GFR føre til?

Ved KNS

A
Maintenance of acid-base balance; As CKD progresses, the kidneys lose their ability to clear organic acids from the body, leading to accumulation in the blood.
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11
Q

Hva vil redusert endokrin aktivitet føre til ved KNS?

A
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12
Q

Hva kan redusert glukoneogense gi ved KNS?

A

Økt risiko for hypoglykemi

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13
Q

Hva kjennetegner mange av pasientene med KNS?

A

Pasienter er ofte asymptomatiske fram til senere stadier av KNS pga. av de eksepsjonelle kompensatoriske mekanismene nyrene har

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14
Q

Hvilke manifestasjoner vil Na+/H2O retensjonen ved KNS ha?

A

Hypertensjon og hjertesvikt

Pulmonal og perifere ødemer:
- Vanligvis interstitielle pulmonale ødem

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15
Q

Hva er uremi?

A
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16
Q

Hvilke konstitusjonelle symptomer kan oppstå pga. uremi?

A
Constitutional symptoms; A collection of nonspecific symptoms such as weight loss, fever, chills, night sweats, changes in appetite, changes in sleep, chronic pain, fatigue, and malaise. Typically evaluated on a review of systems with further evaluation based on pertinent positives and negatives.
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17
Q

Hvilke GI-symptomer kan uremi føre til?

A

Kvalme og oppkast

Nedsatt matlyst

Uremic fetor:
- Karakteristisk ammonium- eller urinlukt fra munnen

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18
Q

Hvilke dermatologiske fenomener kan uremi gi?

A
The exact cause of pruritus is unknown. Hypotheses include accumulation of histamine, deposition of urate crystals, increased levels of parathyroid hormone, neuronal changes, and minor inflammatory reactions.
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19
Q

Hvordan kan uremi føre til serositt?

A
Although the risk of pericarditis correlates with the degree of azotemia (increased retention of urea and creatinine), it does not correlate specifically with increased BUN (Blood urea nitrogen test) or creatinine levels. Since uremic pericarditis does not cause inflammatory cells to invade the myocardium, there are generally no ECG findings.
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20
Q

Hvilke nevrologiske symptomer kan uremi føre til?

A
Asterixis; A brief, low frequency (3–5 Hz), rhythmless tremor of the hand that occurs when the arm is outstretched and the wrist is extended. Seen most commonly in hepatic encephalopathy but also in azotemia and severe hypercarbia.
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21
Q

Hvilke hematologiske symptomer kan oppstå pga. uremi?

A
Studies have shown that administration of desmopressin leads to increased plasma concentrations of vWF and factor VIII. After administration, a shortened bleeding time could be observed in uremic individuals.
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22
Q

Hva viser bildet?

A
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23
Q

Hva viser bildet?

A
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24
Q

Fyll inn figuren

A
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25
Q

Hva er de diagnostiske kriteriene for KNS?

A
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26
Q

Når kan man snakke om en progresjon av KNS?

A
A definite decline is defined as a change to a worse eGFR category AND a ≥ 25% drop in eGFR from baseline. A sustained decline in eGFR of > 5 mL/min/1.73 m2 per year is known as rapid progression.
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27
Q

Hva mener man med ESRD?

A
There is currently no consensus on the definition of ESRD. It is sometimes applied to anyone with CKD category G5 (i.e., eGFR < 15 mL/min/1.73 m2), however, many patients with this degree of renal dysfunction may not develop manifestations of uremia or require renal replacement therapy for several years. Most likely due to associated complications (e.g., anemia of chronic kidney disease) and increased cardiovascular risk factors (e.g., hypertension).
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28
Q

Hvordan klassifiserer man KNS?

A
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29
Q

Hvordan brukes CGA i klinikken, og hvordan kan man tolke dette?

A
Standardized documentation; e.g., “Diabetic kidney disease G3A2." KDIGO guidelines recommend that low to moderate risk patients should be monitored once a year, high-risk patients twice per year, and very high-risk patients three to four times per year.
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30
Q

Hvilke to underpunkter går under årsak ved bruk av CGA?

A
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31
Q

Fyll inn tabellen

A
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32
Q

Hva er målet med den diagnostiske evalueringen ved KNS?

A

Målet med diagnostikken er å bekrefte kronisiteten av nyresvikten og identifisere årsaken til den.

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33
Q

Hvilke parametre på nyrefunksjon bruker man ved diagnostikk av KNS?

A
The CKD-EPI equation is usually preferred, as it has been found to be more accurate than the MDRD equation, especially in patients with a mildly decreased or normal GFR (i.e., GFR ≥ 60 mL/min/1.73 m2). BUN; Blood urea nitrogen test: A blood test that measures the amount of urea nitrogen, a waste product produced by the liver in the urea cycle after protein degradation. Urea nitrogen is physiologically filtered and excreted by the kidneys.
34
Q

Hva er CKD-EPI- og MDRD equation?

A

CKD-EPI:

An equation used to estimate the glomerular filtration rate (eGFR) in patients with chronic kidney disease based on the patient’s serum creatinine and/or cystatin C levels, age, and gender. It is considered to be more accurate than the MDRD equation in patients with normal or mildly decreased renal function (i.e., eGFR ≥ 60 mL/min/1.73 m2).

MDRD:

An equation used to estimate the glomerular filtration rate (eGFR) in patients with chronic kidney disease based on the patient’s age, gender, and serum creatinine level. Useful in patients with an eGFR < 60 mL/min/1.73 m2 but tends to underestimate the true GFR in patients with normal or mildly decreased renal function.

https://next.amboss.com/us/article/lg0vv2?q=chronic+kidney+disease&m=KqbUzu#Zeb975888cde4515672ab89a7a3068ab2

https://next.amboss.com/us/article/lg0vv2?q=chronic+kidney+disease&m=iXXJB9#Zeb975888cde4515672ab89a7a3068ab2

35
Q

Hvilke diagnostiske urinprøver kan man gjøre ved mistanke om KNS?

A
UACR; Urine Albumin to creatinine ratio.
36
Q

Hvilken annen blodprøve er akt. ved KNS?

37
Q

Hvilken bildemodalitet brukes først ved KNS, og hva ser man etter?

A
While increased echogenicity in itself is a nonspecific finding, the combined presence of decreased kidney length and increased cortical echogenicity suggests irreversible kidney disease.
38
Q

Hva viser bildet?

39
Q

Hvilken informasjon er man avhengig av for å finne den underliggende etiologien til KNS?

A

Integrering av informasjon fra pasientens:

Kliniske presentasjon

Labratorietprøver

Bildediagnostikk

Patologisvar

40
Q

Hva tyder på at grunnen til KNS skyldes diabetes, og hvordan kan man us. dette?

A
May be seen with diabetic nephropathy
41
Q

Hva tyder på at grunnen til KNS skyldes glomerulonefritt, og hvordan kan man teste dette?

42
Q

Hva tyder på at årsaken til KNS skyldes myelom, og hvordan kan man teste dette?

43
Q

Hva tyder på at årsaken til KNS skyldes nyrearteriestenose, og hvordan kan man teste dette?

44
Q

Hva tyder på at årsaken til KNS skyldes amyloidose, og hvordan kan man teste dette?

45
Q

Når er det indikasjon for å ta en nyrebiopsi ved KNS?

A
In most patients, the cause of CKD can be inferred from the initial assessment and noninvasive studies; pathological confirmation is usually not required.
46
Q

Hvordan og hvilke intervensjoner kan man behandle pas. med KNS?

A

Ernæringsterapi

Justeringer av medikamenter

Nyreerstatningsterapi

47
Q

Hvordan kan man behandle KNS med ernæringsterapi?

A
Mediterranean diet; Can significantly improve the lipid profile and weight and blood pressure control. Protein restriction; This reduces the risk of ESRD and mortality. A higher protein intake goal of 0.6–0.8 g/kg/day may be considered in patients with diabetes. Sodium restriction reduces blood pressure and helps achieve better volume control; it may also help reduce proteinuria. Patients with CKD are at risk of vitamin B1 deficiency, vitamin B2 deficiency, vitamin B6 deficiency, vitamin C deficiency, vitamin K deficiency, and/or vitamin D deficiency.
48
Q

Hvordan kan medikamentelle justeringer brukes ved behandling av pas. med KNS?

A
Weight the risks and benefits of potentially nephrotoxic substances on a case-by-case basis.
49
Q

Hvilke typer nyreerstatende behandling kan man bruke ved KNS?

A
Refractory deterioration in nutritional status despite optimal dietary interventions. Referral for living donor preemptive renal transplantation may be considered for adult patients with eGFR < 20 mL/min/1.73 m2 and evidence of progressive and irreversible CKD in the past 6–12 months.
50
Q

Hva bør alle pas. med KNS evalueres for?

51
Q

Hvilket systolisk BT bør pas. med KNS ha?

A
Good blood pressure control is essential to prevent atherosclerotic cardiovascular disease (ASCVD). Society and expert panel guidelines vary in their specific recommendations, especially with regards to optimal blood pressure targets. The recommendations below are consistent with the 2021 KDIGO clinical practice guideline for the management of blood pressure in chronic kidney disease. SBP < 130 mmHg; This strict SBP target has been associated with reduced ASCVD risk and all-cause mortality in most patients with CKD. However, the benefit remains uncertain for patients in eGFR categories G4–G5 and those with concomitant diabetes mellitus. Patients with a higher SBP target; E.g., patients with limited life expectancy, significant comorbidities, or symptomatic postural hypotension.
52
Q

Hvilken farmakologisk terapi kan man bruke hos pas. med KNS med forhøyet BT?

A
Depending on the eGFR category, some antihypertensives may require dose adjustments. Avoid any combinations of an ACEI (angiotensin-converting enzyme inhibitors), ARB (angiotensin receptor blocker), and/or direct renin inhibitor because of the increased risk of hyperkalemia and acute kidney injury (ACI).
53
Q

Hvilken ikke-farmakologisk behandling kan man gi til pas. med KNS og forhøyet BT?

A

Livsstilsforandringer!

54
Q

Hva er målet med lipidbehandlingen for pas. med KNS?

A

Redusere atherosklerotisk kardiovaskulær sykdom

55
Q

Hvilke prøver bør man ta for å evaluere lipidnivået hos en pas. med KNS?

A
Lipid panel: A group of laboratory tests used to diagnose and follow-up patients with dyslipidemia, and for the evaluation of cardiovascular risk. Generally includes triglycerides, total cholesterol, HDL, LDL, and non-HDL levels.
56
Q

Hvilken type farmakologisk og ikke-farmakologisk behandling kan man gi pas. med KNS og høye lipidverdier?

A
These recommendations differ from the 2019 recommendations by the American Heart Association and the 2022 USPSTF recommendation on statin use. Lifestyle changes including dietary modifications, weight reduction, reduced alcohol intake, and increased physical activity are recommended, especially in patients with elevated triglyceride levels.
57
Q

Hvordan bør pas. med KNS og diabetes behandles?

A

HbA1c may not accurately reflect glycemic control in patients with CKD and eGFR < 30 mL/min/1.73 m2.

Medications may need to be reduced or stopped as eGFR declines.

SGLT-2 (sodium-glucose co-transporters) inhibitors and GLP-1 (Glucagon-like peptide 1) receptor agonists have been shown to slow CKD progression and reduce urinary albumin excretion and ASCVD events.

58
Q

Hvilke pas. med KNS bør starte med platehemmere?

A
The risk of bleeding in patients without established ASCVD may outweigh the benefits of aspirin.
59
Q

Når er screeningtester for pas. med KNS indisert? Hvem bør man ofte screene?

A
The recommended tests and their frequency can vary and should be tailored to each patient.
60
Q

Gi en oversikt over screeningtester for pas. med KNS?

A
Hyperkalemia; Especially in patients who become oliguric or have other risk factors for hyperkalemia (e.g., high potassium diet, RAAS inhibitor therapy, insulin deficiency). Hyperphosphatemia is caused by decreased urinary phosphate clearance, while hypocalcemia is mediated by hyperphosphatemia and decreased vitamin D production; this is because earlier in the disease course, mild imbalances tend to be normalized by a reactive rise in PTH levels (i.e., secondary hyperparathyroidism). Vitamin D; Calcidiol levels reflect total body vitamin D stores and ↓ calcitriol due to decreased renal conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D; may be seen with any stage of CKD and worsens as GFR declines. ABG; The kidneys are often no longer able to maintain acid-base balance when the GFR drops below 30 mL/min/1.73 m2. An accumulation of hydrogen ions leads to acidosis.
61
Q

Hvilke akutte komplikasjoner forekommer ved KNS?

A
Pulmonary edema; Due to an inability in patients with very low GFR to clear excess fluids. Hyperkalemia; May be triggered by excessive dietary potassium, nonadherence to diuretic therapy, or a new medication or medication interaction (e.g., ACE inhibitors, potassium-sparing diuretics). Patients with CKD have a higher risk of infection than the general population. Drug toxicity; Due to impaired renal excretion and the effect of changes in volume status and plasma protein binding on volumes of distribution.
62
Q

Hva er calciphylaxis?

A

Definition:

A rare but potentially life-threatening condition characterized by dermal and subcutaneous arteriolar calcifications that cause painful skin necrosis.

63
Q

Hvilke pasienter er i faresonen for å utvikle calciphylaxis?

A

Most commonly seen in patients with ESRD who are receiving dialysis.

Comorbidities: diabetes mellitus, obesity, CKD-mineral and bone disorder, warfarin therapy.

64
Q

Hva kjennetegner klinikken ved calciphylaxis?

65
Q

Hvordan diagnostiserer man calciphylaxis?

66
Q

Hvilke diff.diagnoser har man til calciphylaxis?

67
Q

Hvordan er behandlingen av calciphylaxis?

A
Evidence from clinical trials is largely lacking given the rarity of calciphylaxis. Treatment recommendations are based on expert opinion and observational data. MTC; Including nephrology, dermatology, wound care, nutrition, palliative care. Sodium thiosulfate is thought to inhibit vascular calcifications and is the most commonly used agent to treat calciphylaxis. The data supporting its use is from small case series and observational studies.
68
Q

Hva viser bildet?

69
Q

Hva er patofysiologien til anemi ved KNS, og hva er typiske lab funn?

A
Anemia is worsened by uremia because uremia induces hemolysis and coagulopathies and inhibits erythropoiesis. In patients > 15 years of age with CKD, anemia is defined as an Hb level of < 13.0 g/dL in male individuals and < 12.0 g/dL in female individuals. MCV may be low if there is concurrent iron deficiency.
70
Q

Hvordan behandler man anemi hos pas. med KNS?

A
The decision to initiate therapy with ESAs should be made on a case-by-case basis, considering factors such as the rate of fall of Hb concentration, risk of requiring a transfusion, the presence of signs of anemia, and the need for renal replacement therapy. Measure Hb frequently: every month initially and at least every 3 months once Hb levels are stable. Consider for patients with severe anemia, symptomatic patients who do not respond to ESA therapy, and those in need of rapid preoperative Hb correction.
71
Q

Hva er CKD-MBD?

A
CKD-MBD; Chronic kidney desease-mineral and bonde disorder.
72
Q

Hvordan er patofysiologien til CKD-MBD?

A
Calcium phosphate precipitation; dannelse av kalsiumfosfat i vev.
73
Q

Hva er den histologiske klassifikasjonen av CKD-MBD?

74
Q

Hva er de kliniske kjennetegnene ved CKD-MBD?

75
Q

Hvordan diagnostiserer man CKD-MBD?

A
Due to increased osteoclast function, particularly in the setting of severe PTH elevation. Especially for patients with other risk factors for osteoporosis and only when the results will affect management.
76
Q

Hvordan er behandlingen av CKD-MBD?

A
Calcitriol; May be used for patients with CKD category G4–G5 who have progressive and severe hyperparathyroidism.
77
Q

Hvilke komplikasjoner kan KNS få for barn?

78
Q

Hva kjennetegner KNS hos gravide?

A
The risk of complications increases with the degree of the concomitant kidney dysfunction.
79
Q

Hvilke maternelle og føtale komplikasjoner kan oppstå pga. KNS hos gravide?

80
Q

Hvordan behandler man KNS hos gravide?

A

Patients should be cared for by a multidisciplinary team, including nephrologists, neonatologists, and health care personnel specialized in high-risk obstetrics.

Optimization of blood pressure (i.e., < 140/90 mm Hg) to reduce the risk of preeclampsia and other complications.

Minimization of proteinuria: Treatment depends on the underlying etiology (e.g., pregnancy-safe immunosuppression with prednisone or calcineurin inhibitors in lupus nephritis).

Consideration of anticoagulation in individuals with severe proteinuria.

Prevention of preeclampsia with aspirin before 16 weeks of gestation and calcium and vitamin D supplementation throughout the pregnancy.

81
Q

Gi en oppsummering når det kommer til KNS

Nefrologi (17 decks)

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