Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2612_Библиотеки_им_академика_М_И_Перельмана
.pdf
7 Kidney medicine
Urine microscopy
https://t.me/med1917
Urine microscopy is operator dependent and many consider it to be a dying art.
Cells
Red blood cells:
• >2 red cells/ mm3 is a bnorm al.
• Can come from anywhere in the urinary tract. Isomorphic red cells are similar to
circulating red cells and suggest bleeding from an extrarenal source. Dysmorphic
red cells are abnormal in size/ shape. Although they may indicate bleeding from
the glomerulus (especially in exam questions), assessment is subjective and
dysmorphism also occurs due to changes in pH, osmolality, protein, and due to
tubular passage.
White blood cells (
• >10 whi te cel ls/ mm3 or 3 or m ore whi te cel ls/ high power film are abnormal.
• Causes include
crosis, diabetes, kidney transplant rejection, malignancy, calculi,
Squamous epithelial cells:
• Often seen, not pathological.
fig
7.2a
):
UTI
, glomerulonephritis, tubulointerstitial nephritis, papillary ne-
STI
.
Casts
• Casts are cylindrical bodies formed in the lumen of distal tubules. They are formed
of Tamm– Horsfall protein combined with cells.
• Hyaline casts (fig
• Red cell casts (fig
glomerulus, eg glomerulonephritis (
• White cell casts (fig
nephritis (
• Granular casts (fig
7. 2 b
)— seen in normal urine, fever, exercise.
7. 2 c
)— signify an inflammatory process causing bleeding in the
p
7. 2 d
p
307
)— pyelonephritis, interstitial nephritis (p
).
7. 2 e
)— formed from degenerated tubular cells, non- specific in
307
).
314
), glomerulo-
kidney disease.
Crystals
Crystals are common in old or cold urine and may not signify pathology. They are
important in renal stone disease.
• Uric acid (fig
• Calcium oxalate (fig
diet, ethylene glycol poisoning.
• Cystine (fig
(a)
7. 2 f
, and p
672
)— stones, tumour lysis syndrome.
7. 2 g
)— stones (p
7. 2 h
)— cystinuria (p
(b) (c) (d)
630
), oxalate nephropathy (p
317
).
315
), high oxalate
291
(e) (f) (g) (h)
Fig 7.
2
(a) White cells; (b) hyaline cast; (c) red cell cast; (d) white cell cast; (e) granular cast;
(f) uric acid crystals; (g) calcium oxalate crystals; (h) cystine crystal.
Images (a) to (h) reproduced from Turner et al., Oxford Textbook of Clinical Nephrology,
2005
permission from Oxford University Press.
, with
7 Kidney medicine
Urinary tract infection (
UTI
UTI
https://t.me/med1917
292
Definitions Bacteriuria Bacteria in the urine. May be asymptomatic or symp-
tomatic. Bacteriuria is not a disease.
features including:
Upper
UTI
symptom relief and/ or prevention of complications.
syndrome
Lower
infection of kidney/ renal pelvis (pyelonephritis). The aim of treatment is
Diagnosis of exclusion in patients with dysuria and frequency, without
demonstrable infection.
Incidence Annual incidence of
have asymptomatic bacteriuria (>
assessment is mandatory). Pyelonephritis =
Classification
• Uncomplicated: normal renal tract structure and function.
• Complicated: structural/ functional abnormality of genitourinary tract, eg ob-
struction, catheter, stones, neurogenic bladder, kidney transplant.
Risk factors
• Bacterial inoculation Sexual activity, urinary/ faecal incontinence, constipation.
• Binding of uropathogenic bacteria Spermicide use, oestrogen, menopause.
• Urine flow Dehydration, obstructed urinary tract (p
• Bacterial growth DM, immunosuppression, obstruction, stones, catheter, renal
tract malformation.
Symptoms
• Key symptoms Dysuria, new nocturia, cloudy urine.
• Other symptoms Urgency, frequency, suprapubic tenderness, haematuria
• Prostatitis Pain: perineum, rectum, scrotum, penis, bladder, lower back. Fever,
malaise, nausea, urinary symptoms, swollen or tender prostate on
• Acute pyelonephritis Fever, rigor, vomiting, loin pain/ tenderness, costovertebral
pain, associated cystitis symptoms, myalgia, septic shock.
Signs Suprapubic/ loin tenderness, fever. Check for a distended bladder/ enlarged
prostate. If vaginal discharge,
Te st s
• Dipstick Not needed if two or three key symptoms. Use in <65yrs if one key
or other symptoms. Nitrites make
diagnoses equally likely. Less useful in ♂. Do not use >
catheterized sample.
•
MSU
culture Conventional cut o >
tomatic best diagnostic criterion may be >
positive dipstick and risk of resistance or leucocyte only positive, >
nancy. If catheterized and new urinary symptoms (not cloudy urine), change catheter first.
• Blood tests If systemic symptoms:
10– 25
% of pyelonephritis). Treat sepsis. Consider fasting glucose.
• Imaging Consider
dynamics,
UTI,
plained
CT
) in pyelonephritis, failure to respond to treatment, recurrent unex-
unusual organism, prostatitis, persistent haematuria.
Organisms Usually anaerobes and Gram- negative bacteria from bowel and va-
ginal flora. E. coli is the main organism (
Staphylococcus saprophyticus (a skin commensal) in
such as Proteus mirabilis and Klebsiella pneumonia. For sterile py uria s ee
Table 7.
2
Causes of sterile pyuria (numbers of white cells but sterile with standard culture)
Infection related Non- infection related
TB Calculi Polycystic kidney
Recently treated
Inadequately treated
Fastidious culture requirement Tubulointerstitial nephritis
Appendicitis, prostatitis, chlamydia Chemical cystitis Drugs, eg steroids
UTI
)
UTI
infection of bladder (cystitis), prostate (prostatitis);
1 A combination of bacteriuria and clinical
Abacterial cystitis/ urethral
Urethritis See pp
UTI
80
USS
and referral to urology for assessment (cystoscopy, uro-
408–9
.
in ♀ is 10– 20%. 10% of ♂ and 20% of ♀ >65 years
65
yea rs
MSU
is not diagnostic in isolation and clinical
3
per
1000
pat ient- years.
632
).
PR
(p
637
% do not have
104–
FBC, U&E, CRP
UTI,
consider
PID
(p
409
).
UTI
more likely. If only leucocytes then other
65
yrs. No diagnostic value in
105 colony- forming units (cfu)/ mL but if symp-
102–
103cfu/ mL. Send in <65yrs if nitrite-
65
yrs, ♂, preg-
, and blood culture (positive in only
70– 95
% in community but in hospital).
5– 10
%. Other Enterobacteriaceae
table
UTI
Renal tract tumour Recent catheter
Papillary necrosis Pregnancy
SLE
.
).
7. 2
.
7 Kidney medicine
Managing
https://t.me/med1917
UTI
Do not use antibiotics for the treatment of asymptomatic bacteriuria in non-
pregnant , , and adults with catheters.
Treatment should be based on culture/ sensitivity results, according to local
guidance. The below is merely a guide.
Non- pregnant women
• Self- care advice for all: fluid intake, analgesia (evidence for cranberry/ alkali).
• May not need immediate antibiotic depending on severity and risk of complications.
Back- up antibiotic if worsening symptoms or no improvement within
• First- line: 3- day course of nitrofurantoin MR (e
200
mg BD. Alternative: pivmecillinam
3
fosfomycin
g single dose.
GFR
400
mg stat, then
>45)
100
200
48
h.
mg BD or trimethoprim
mg
TDS
for 3 days or
Pregnancy
• Trea t
UTI
and asymptomatic bacteriuria due to risk of pyelonephritis and preterm
7
- day course of antibiotics recommended.
delivery.
• First- line: nitrofurantoin
100
mg BD if p re- pregnancy e
GFR
>45 and remote from term
(neonatal haemolysis). Alternatives: amoxicillin (if sensitive), cefalexin.
Men
• Trea t wi th a 7- day course of trimethoprim
GFR
>45 and no cli nical suspi cion of prost atitis ).
e
• If prostatitis then needs 14- day course with review for ongoing treatment.
200
mg BD or nitrofurantoin
100
mg BD (if
Options: ciprofloxacin, ofloxacin, trimethoprim, co- trimoxazole.
Pyelonephritis
• Trea t i n h os pi ta l i f s us pi c io n o r r is k ( im mu no su pp re ss io n, DM) of sepsis, unable to
tolerate oral medication/ fluid, recurrence, abnormal renal tract, pregnancy.
• Antibiotic options: cephalexin, co- amoxiclav, trimethoprim (not in 1st trimester),
ciprofloxacin (avoid in pregnancy).
Catheter associated
• Remove/ change catheter if in place for >7 days .
• Cloudy urine is not a useful sign. Exclude alternative focus of infection/ cause of de-
lirium in the absence of new urinary symptoms.
Urinary tract tuberculosis
• Sterile pyuria, dysuria, frequency, suprapubic pain but negative standard culture. Ask about malaise, fever, night sweats, weight loss, back/ flank pain, visible
haematuria.
• Can also cause an interstitial nephritis (p
nephritis is rare.
• Diagnose by microscopy with acid- fast techniques (sensitivity) and mycobacterial
culture of an early morning
• Tre at ac co rd in g t o l oc al gu id an ce , t yp ic al ly ri fa mp ic in an d i so ni a zi d fo r 6 months,
MSU
with pyrazinamide and ethambutol for
314
) and amyloidosis (p
and / or urinary tract tissue.
2
mon ths (p
390
).
311
). Glomerulo-
The ‘piss prophets’
Beware the fallacies, deceit and juggling of the piss- pot science used by all those
who pretend knowledge of diseases by the urine.
Thomas Brian,
1655
Medieval texts1 give the following maxims regarding urinary change and disease:
• White or straw- coloured urine = weak and cold liver and stomach.
• Foamy urine = eructation (belching).
• Light- coloured, turbid urine = mucus.
• Lead circle on thin urine = pathological melancholy.
• Bubbles on the surface = disease of the head.
• Watery urine = love sickness.
• Swampy, black, stinking urine = fatal.
• Lead- coloured urine = a disintegrating uterus.
• Reddish, cloudy urine with bubbles = asthma or an irregular heartbeat.
293
.
1
Uroscopy in Early Modern Europe by Michael Stolberg, Routledge,
2016
, pp53– 6.
7 Kidney medicine
Acute kidney injury (
AKI
https://t.me/med1917
294
Definition
Acute kidney injury (
serum creatinine or urine output, occurring over hours– days. It includes dierent
aetiologies and may be multifactorial.
AKI
definitions have been amalgamated into a single definition and staging system.
Kidney Diseases: Improving Global Outcomes (
• Rise in creatinine >
• Rise in creatinine >1.5 × baseline (pre-
• Urine output <0.5mL/ kg/ h for >6 consecutive hours.
The severity of
of oliguria (
Table 7.
Stage Serum creatinine Urine output
1
2 2.0– 2.9
3
AKI
is then staged according to peak creatinine or period/ severity
table
7. 3
3
). A clinical approach to
KDIGO
staging system for
>26.5µmol/ L (0.3mg/ dL) or
1.5– 1.9
× baseline
× baseline <0.5mL/ kg/ h for >12h
>
353.6
µmol/ L (4.0mg/ dL) or
3.0
× baseline or
>
new renal replacement therapy
Limitations Serum creatinine does not rise above the upper reference limit until up
50
% of kidney function is lost. It is also aected by non- glomerular factors: muscle
to
mass, protein intake, tubular secretion, pregnancy. But other
NGAL
) have failed to demonstrate superiority over serum creatinine to date.
Epidemiology
AKI
aects up to 18% of hospital patients and ~1 in 3 patients in intensive care.
Risk factors for
AKI
include pre- existing
cular disease, malignancy, chronic liver disease, complex surgery).
Causes
Commonest causes:
1
Sepsis.
2
Cardiogenic shock.
3
Hypovolaemia: haemorrhage,
4
Nephrotoxic medication.
5
Renal tract obstruction.
6
Hepatorenal syndrome.
Aetiology can be divided according to site (
• Pre- renal: perfusion to the kidney.
• Renal: intrinsic kidney disease.
• Post- renal: obstruction to urine (bilateral if two working kidneys, unilateral if
single functioning kidney).
Table 7.
4
Aetiology of
Where? Pathology Example
Pre- renal Vascular volume
Renal
Post- renal Within renal tract Stone, renal tract malignancy, stricture, clot
Cardiac output
Systemic vasodilation Sepsis, drugs
Renal vasoconstriction
Glomerular (
Interstitial (
Vessels
Extrinsic compression Pelvic malignancy, prostatic hypertrophy, retro-
): a clinical approach
AKI
) is a syndrome of decreased kidney function, measured by
KDIGO
26.5
µmol/ L within 48h or
AKI
D&V
AKI
pp
306–7
) Glomerulonephritis,
p
314
)
) guidelines2 define
AKI
) within 7 days or
AKI
is shown in fig
<
0.5
mL/ kg/ h for 6– 12h
0.3
mL/ kg/ h for >24h or
<
anuria for >
CKD
, age, and comorbidity (
12
AKI
, diuresis, 3rd space, eg pancreatitis.
table
7.4
) as:
Haemorrhage,
Cardiogenic shock,
NSAID
hypoperfusion causing intrinsic kidney damage)
Drug reaction, infection, infiltration (eg sarcoid)
Vasculitis,
peritoneal fibrosis
S,
ACE- i, ARB
D&V
HUS, TTP, DIC
, burns, pancreatitis
MI
, hepatorenal syndrome
ATN
(prolonged kidney
AKI
7. 3
.3
h
biomarkers (eg
DM,
cardiovas-
as:
KIM- 1
,
7 Kidney medicine
NEWS (see p
https://t.me/med1917
876
, fig A1)
Consider critical care referral
295
Fig 7.
3
The clinical approach to
Referring to a nephrologist
Request that advice/ review is necessary due to:
•
AKI
not respon ding t o treat ment.
•
AKI
wit h comp licat ions: K+ , acidosis, fluid overload, hypertension.
• Stage 3
AKI
(table
7. 3
•
AKI
wit h dicult fluid balance (eg hypoalbuminaemia, heart failure, pregnancy).
•
AKI
due to pos sible intrin sic kidney disea se (table
•
AKI
wit h hyper tensi on.
).
Know Ba sel ine crea tin ine and tre nd ( not e
carbonate/ lactate, Hb, platelet count (+ film), urin e dip (before catheter), observa-
(NEWS)
tions
USS
s in c e a d mi s si o n , fl u id i np u t/ output, examination (hypo/ hypervolaemia),
result, comorbidity ( eg DM), drugs given (what? when? nephrotoxic?).
AKI
.
3
7.4
).
GFR
wh ich is o nly for stea dy s tat e), K+ , bi-
7 Kidney medicine
Acute kidney injury (
AKI
https://t.me/med1917
296
Management of
• Pre- renal: correct volume depletion and/ or kidney perfusion via circulatory/ car-
diac support, treat underlying sepsis, stop drugs causing hypotension.
• Renal: refer for diagnosis (biopsy) and treatment of intrinsic kidney disease.
• Post- renal: catheter, nephrostomy, urological intervention.
AKI
requires diagnosis and treatment of the underlying aetiology:
Common to all aetiologies of
kalaemia, and the timely recognition of those who require renal replacement (
Fluid balance
Vol ume sta tus
• Hypovolaemia: pulse,
turgor, capillary refill, daily weight loss.
• Overload: BP,
JVP
Hypotension may be relative if old age, vascular stiness, chronic hypertension
JVP
does not reflect intravascular volume if right- sided heart disease/ failure.
BP,
skin turgor, capillary refill changes may be late— do not wait for them.
Hypovolaemia, fluid resuscitation
• If hypovolaemic, kidney perfusion requires volume replacement.4
• Care in cardiac disease (kidney perfusion despite adequate circulating volume)
and sepsis/ third- spacing (extravascular volume).
• Dynamic assessment is essential: examine before and after fluid is given to ensure
an adequate response and to reduce the risk of fluid overload.
1
Give
500
4
mL crystalloid over 15min.
2
Reassess fluid state. Get expert help if unsure or if patient remains shocked.
3
Further boluses of
Stop when euvolaemic or seek expert help if 2L given without response.
Which crystalloid? Any crystalloid can be used (follow local guidelines). 0.9%
(‘normal’) saline is non- buered, contains chloride, and may cause hyperchloraemic
acidosis. ‘Balanced’ crystalloids include Hartmann’s, Ringer’s lactate, and Plasma- Ly te
They a re clo ser in compo sitio n to ext racell ular fl uid an d are o ften us ed pre ferent ially.
What about colloid? Blood components should be used in resuscitation due to
haemorrhage. Human albumin solutions may be given only under specialist advice
in hepatorenal syndrome. Colloids do not improve mortality in the critically ill.
Hypervolaemia, fluid overload
Occurs due to aggressive fluid resuscitation, oliguria, and in sepsis due to capillary
permeability. Monitor weight daily in patients receiving
• Oxygen supplementation if required.
• Fluid restriction including oral and IV volumes. Give antibiotics in minimal fluid and
consider concentrated nutritional support preparations.
• Diuretics in symptomatic fluid overload.
Do not use diuretics to treat oliguria without fluid overload.
• Renal replacement therapy (p
referral to nephrology/ critical care.
Acidosis
• Mild = pH 7.30– 7.36 (~bicarbonate >20mmol/ L).
• Moderate = pH 7.20– 7.29 (~bicarbonate 10– 19mmol/ L).
• Severe = pH <7.2 (~bicarbonate <10mmol/ L): refer to nephrology/ critical care.
Treatment is of the underlying disorder to stop acid production. If treatment is
delayed, acidosis will persist and renal replacement may be needed (
Bicarbonate in acute acidosis is controversial. Adequate ventilation is needed to
prevent respiratory acidosis. A sodium load may also precipitate fluid overload in
vulnerable patients.
Chronic acidosis is treated in
CKD
benefit in
progression.
): management
AKI
are management of fluid balance, acidosis, hyper-
BP,
postural BP drop, urine volume, non- visible
, RR,
O
sat uratio n, lun g crepi tatio ns, oe dema, gallo p rhyth m.
2
250– 500
mL crystalloid with clinical review after each.
IV
flu ids. Tre at wi th:
302
). Oligo/ anuric
CKD
with bicarbonate <22mmol/ L due to evidence of
AKI
with fluid overload needs urgent
p
JVP
302
p
297
, tissue
).
).
.
®
.
7 Kidney medicine
Hyperkalaemia
https://t.me/med1917
Fig 7.
4
ECG changes with severe hyperkalaemia; note broad QRS complexes.
ECG
changes In order: tall ‘tented’ T waves; increased PR interval; small or absent P
wave; widened
erable inter- individual susceptibility.
QRS
complex (fig
Don’t wait for a lab result: use point- of- care (blood gas) testing if available.
Treat5 if K+ >6.5mmol/ L or
1
Protect the heart 10mL of 10% calcium chloride2 (or 30mL of 10% calcium
gluconate)
This is cardioprotective (for
2
Shift K
IV
over 5– 10
+
10U soluble insulin in 25g glucose (e.g
lin stimulates intracellular uptake of K
(varies with kidney function and
Salbutamol can be used in addition but high doses are required:
SE
nebulizer (
3
Remove K
changes H
ble out- patients but
is within
: tremor, palpitations, headache).
+
Sodium zirconium cyclosilicate is a non- absorbed binder that ex-
+
+
and Na
1
h, lowering serum K
and patiromer have slower onsets of action (
treatment. Renal replacement may be indicated. Safe inter- hospital transfer
+
requires K
4
Monitor K
2– 3.5h after insulin (up to 6h in
treatment blood glucose
5
Prevent recurrence Withhold drugs which K
<6.5mmol/ L— discuss with nephrology and critical care.
+
and glucose. Hypoglycaemia occurs in 11– 75
amiloride, eplerenone, trimethoprim, digoxin (remember to re- start when safe).
IV
sodium bicarbonate is not routinely used in the treatment of
weigh (unproven) benefit. Follow local guidelines in hyperkalaemic cardiac arrest.
Renal replacement therapy (
RRT
options in
dialysis is rare for
AKI
include haemodialysis and haemofiltration (p
AKI
in adults and in high- income countries but can be used. No
clear benefit has been demonstrated for any
is preferred if haemodynamic instability, acute brain injury, or cerebral oedema.
Possible in dications for
• Symptomatic fluid overload unresponsive to medical treatment.
• Severe/ prolonged acidosis.
• Recurrent/ persistent hyperkalaemia despite medical treatment.
• Uraemia, eg pericarditis, encephalopathy (more likely if underlying
The decision to start
not wait for them to occur. Fluid overload is a predictor of worse outcomes.
Possible complications of
RRT
ance, procedural hypotension, bleeding, altered nutrition, and drug clearance.
2
Calcium chloride contains 3× calcium than the same volume of gluconate. Concern exists about the
bioavailability of calcium gluconate
7.4
); ‘sine wave’ pattern; asystole. There is consid-
The
ECG
may be normal
ECG
changes (look at an
min, repeated if necessary and if
30– 60min) but does not treat K
+
DM
) over 30– 60
ECG
for all K+ >6.0mmol/ L):
125
mL of 20% glucose) IV. Insu-
, lowering serum K
min and works for up to 2h.
ECG
changes persist.
+
concentration.
+
by 0.65– 1.0
mmol/ L
10– 20mg via
+
for K
and ammonium in the gut. Data come from sta-
10
g
TDS
is approved for use in the acute setting. Onset
+
by 1.1mmol/ L within 48h. Calcium resonium
>4
h) so utility is limited in acute
%, most commonly at
CKD
). Consider 10% glucose IV at 50mL/ h if pre-
<7.0
RRT
mmol/ L.
RRT
) in
AKI
+
:
ACE- i, ARB
, spironolactone,
+
K
as risks out-
302
). Peritoneal
RRT
modality though haemofiltration
CKD
).
is individualized. The aim is to prevent complications: do
RRT
Risks of dialysis catheter insertion and mainten-
.
Both salts carry a risk of tissue necrosis with extravasation.
297
7 Kidney medicine
Chronic kidney disease (
CKD
https://t.me/med1917
298
)
Definition Abnormal kidney structure or function, present for >3 months, with im-
plications for health.
Classification Based on
a marker of kidney damage (
(Problems with e
Table 7.
5
Classification of
Category
G1
G2
G3A
G3B
G4
G5
Table 7.
6
Classification of
6
GFR
category (table
table
GFR
formulae used to stage kidney disease, p
CKD
Notes
GFR
>
90
Only
pathology on biopsy/ imaging, tubule disorder, transplant
60– 89
45– 59
Mild– moderate
30– 44
Moderate– severe
15– 29
Severe
Kidney failure
<
15
CKD
7. 6
by
GFR
(mL/ min/ 1.73m2)
CKD
if other evidence of kidney damage: protein/ haematuria,
GFR
by albuminuria
7.5
), the presence of albuminuria as
), and the cause of kidney disease (table
GFR
GFR
661
Category Albumin excretion (mg/ 24h) Albumin:creatinine ratio (ACR) (mg/ mmol)
A1
A2
A3
Table 7.
7
Classification of
Kidney pathology
Glomerular Minimal change, membranous Diabetes, amyloid
Tubulointerstitial
Blood flow/ vessels Kidney limited vasculitis
Congenital/ genetic Renal dysplasia Alport syndrome, Fabry disease
Transplant Recurrence of primary kidney
<
30
<
3
30– 300 3– 30
>
300
CKD
based on underlying disease
>
30
Examples
Primary kidney disease Systemic disease
UTI
, pyelonephritis, stones
Drugs, toxins, sarcoid
Heart failure,
Calcineurin inhibitor toxicity
disease
Epidemiology 10% of adults and up to 45
Commonest aetiologies: diabetes, glomerulonephritis,
GFR
and albuminuria are independently associated with an risk of:
• All- cause mortality.
• Cardiovascular mortality.
• Progressive kidney disease and kidney failure.
•
AKI.
Patients with
outcomes in
uria categories (
CKD
are more likely to die of
CKD
can be represented as a ‘heat map’ according to
fig
7.5
).
000
premature deaths per year in UK.
BP
/ renovascular disease.
CVD
than to need
RRT.
The risk of adverse
.)
TTP
GFR
and albumin-
7.7
).
Fig 7.
5
Composite risk of adverse outcome by GFR and albuminuria.
Reprinted from Kidney International, 80, AS Levey et al., Chronic kidney disease: definition,
classification, and prognosis,
17– 28, 2011
, with permission from Elsevier.
7 Kidney medicine
The patient with
CKD
https://t.me/med1917
CKD
History
• Does the patient really have
Consider non- steady state, eg
centration but not
Evide nce of chronicity >
• Possible cause Ask about
GFR
symptoms, renal colic. Check drug history and when medications started. Family
history including kidney disease and subarachnoid haemorrhage. Systems review: look out for more than immediately obvious, consider rare causes, ask about
eyes, skin, joints, symptoms suggestive of systemic disorder (‘When did you last feel
well?’), and malignancy.
• Current state Patien ts may o r may not have sym ptoms o f
common once e
GFR
<15: fluid overload (
restless legs, fatigue, pruritus, bone pain, amenorrhoea, impotence.
Examination
• Periphery Oedema, signs of peripheral vascular disease or neuropathy, vasculitic
rash, gouty tophi, joint disease. Arteriovenous fistula (thrill, bruit, recent needling?).
Signs of immunosuppression: bruising from steroids, skin changes/ malignancy.
Uraemic flap/ encephalopathy are late signs.
• Face Anaemia, xanthelasma, yellow tinge (uraemia), jaundice (hepatorenal),
gum hypertrophy (ciclosporin), Cushingoid (steroids), periorbital oedema (nephrotic syndrome), taut skin/ telangiectasia (scleroderma), facial lipodystrophy
(glomerulonephritis).
• Neck
JVP
• Cardiovascular
• Respiratory Pu lmona ry oedema or e usion.
• Abdomen PD catheter or scars from previous catheter (small scars just below um-
for fluid state, tunnelled line (small scar over internal jugular vein and a
larger scar in ‘breast pocket’ area), parathyroidectomy scar, lymphadenopathy.
BP,
sternotomy, cardiomegaly, stigmata of endocarditis. If right-
sided heart failure/ tricuspid regurgitation,
bilicus and to side of midline), signs of transplant (scar, palpable graft), ballotable
polycystic kidneys ± pal pable liver.
Investigation
• Blood Serum creatinine and
normocytic anaemia)
,
Directed investigation for intrinsic kidney disease:
antibodies, serum light chains and paraprotein, complement, cryoglobulin, antihepatitis serology, anti-
• Urine Dipstick (may not de tect al bumin ), u
• Imaging
USS
for anatomy, size, symmetry, corticomedullary dierentiation (non-
specific), and to exclude obstruction.
infiltrative disorders (amyloid, myeloma),
renovascular disease. Isotope scans are more sensitive for scarring.
• Histology Consider kidney biopsy (p
with kidney involvement, progressive disease,
vious cause.
DM
may no t need bi opsy unless atypical, ie haematuria, systemic symp-
toms, no other microvascular disease (retinopathy/ neuropathy).
Monitoring kidney function in
Consider patient view/ preference.
least annually, according to risk. If high risk, monitor every
ange); if very high risk, monitor at least every
GFR
in e
min/
stage with e
1.73
m2/ yr.
GFR
Risk factors for disease progression BP, DM, proteinuria, metabolic disturbance,
volume depletion, infection,
AKI
: treat illness promptly, monitor fluid balance and kidney function.
: a clinical approach
? Does the e
AKI,
drugs (eg trimethoprim alters creatinine con-
), pregnancy (e
3
mon ths— is there a previous creatinine on record?
BP, DM, IHD, UTI
U&E
(compare with previous), Hb (normochromic,
glucose (DM), Ca
PLA2R
. (
ESR
is n ot sen sitive , in
306
CKD
GFR
GFR
reflect the true
GFR
formulae underestimate), malnutrition.
, lower urinary tract symptoms, systemic
CKD
SOB
, oedema), anorexia, nausea, vomiting,
JVP
may n ot refl ect flui d stat e.
2
+
3
, PO
4
ANA,
ACR/ uPCR, MC&S
CKD
kidneys may be small (<9cm) except in
APKD
, and DM. If asymmetrical consider
. Symptoms are more
−
,
PTH
(renal osteodystrophy).
ds
DNA, ANCA
, antiphospholipid
CKD
and protei nuric states .)
(p
290
).
) in nephrotic syndrome, systemic disease
AKI
wit hout recov ery,
CKD
and albuminuria should be monitored at
6
3– 4
mon ths (fig
months (fig
7. 5
, red). A change
≥ 25% is significant. Rapid progression is e
NSAID
S, smoking, obstruction. Risk of superimposed
GFR
(p
661
GBM
wit hout ob-
7. 5
, or-
GFR >
15
mL/
299
)?
,
7 Kidney medicine
Chronic kidney disease (
CKD
CKD
https://t.me/med1917
300
CKD
encompasses a range of disease from mild disease without progression to ad-
vanced, symptomatic disease requiring renal replacement.
CKD
Management of
1
Information and education for people with
2
Treatment to slow kidney disease progression.
3
Treatment of complications of
4
Management of cardiovascular risk in
5
Preparation for renal replacement therapy (dialysis/ transplantation) (p
6,7 requires:
Referral to nephrology
• 5- year risk of renal replacement >5% using four- variable Kidney Failure Risk
https:// kidney fail urer isk.co.uk
Equation:
• Moderate proteinuria u
• Proteinuria u
• Kidney disease progression:
• Hypertension despite four agents, or suspected renal artery stenosis.
• Known or suspected rare or genetic cause of
ACR
• e
GFR
by ≥25% + e
• Sustained e
>30mg/ mmol with haematuria.
GFR >
Tre at me nt t o sl ow ki dn ey d is ea se p rog re ss io n
BP uACR
<70: systolic <
DM
or u
ACR
≥70: systolic <
Renin– angiotensin inhibition Oer treatment with a renin– angiotensin system an-
(ACE-
i,
ARB)
ACR
>3mg/ mmol.
with u
for:
ACR
>70mg/ mmol.
tagonist
• DM and u
• Hypertension and u
• Any
CKD
Do not combine agents due to risk of hyperkalaemia and hypotension. Check K
and kidney function prior to, and
in dose. Stop if K
sible causes of e
SGLT2
inhibitors e
DM
(insucient data in polycystic kidney disease and after a kidney transplant).
+
>6mmol/ L, e
GFR
GFR >25
This is a fast- moving field: check up- to- date e
Glycaemic control in DM Target HbA1c of ~53mmol/ mol (7.0%) unless risk of hypo-
glycaemia, comorbidity, or limited life expectancy.
Lifestyle Exercise, healthy weight, and smoking cessation. Salt intake should be
reduced to <
2
g of sodium/ day (≤5g sodium chloride/ day).
Tre at me nt o f c om pl ic at io ns o f
Anaemia Investigate (especially if anaemic with e
ciencies: iron (hypochromic red cells >
ferrin saturation <
blood loss.
ESA
agent (
20
IV
iron therapy may be needed. Treat with an erythropoietic stimulating
, ‘Epo’) to maintain Hb
ment is due to anti- erythropoietin antibodies and usually causes Hb <
very rare: exclude more likely causes of anaemia first. Avoid blood transfusions
whenever possible, especially if kidney transplantation is predicted. Care with
in sickle cell disease as may increase sickle cell %.
Acidosis Consider sodium bicarbonate supplements for patients with e
low serum bicarbonate (<
Oedema Restrict fluid and sodium intake if clinically indicated. Loop diuretics can
be used. A high dose may be required in advanced
combination can be potent: distal tubule sodium excretion (and inhibition by a thiazide) is increased when treated with a loop diuretic (
fluid state and kidney function.
): management
CKD
.
CKD
.
CKD
.
ACR
>70mg/ mmol unless due to DM and already treated.
GFR
cat egory wit hin 12 mon ths (table
15
mL/ min/ 1.73m2 wit hin 12 mon ths.
CKD
140
mmHg (range
130
mmHg (range
ACR
>30mg/ mmol.
and use lowest tolerated dose.
+ u
ACR
%, ferritin <
22
mmol/ L). Caution in hypertension and fluid overload.
120– 139
mmHg) and diastolic <90mmHg.
120– 129
1– 2
weeks after starting treatment, or a change
GFR
>25%, or creatinine >30%: exclude other pos-
>25 + type 2 DM (caution
GFR
, u
6
%, reticulocyte Hb content >29pg, trans-
100
mcg/ L),
B
, and folate. Do not miss chronic
12
100– 120
g/ L. Pure red cell aplasia with
7. 5
).
.
) and diastolic <80mmHg.
DKA
ACR,
and disease criteria for use.
GFR
>60) and treat other defi-
CKD
. A loop and thiazide diuretic
fig
7.13
, p
312
302
) or
CKD
not due to
ESA
treat-
60
g/ L. It is
GFR
<30 and
). Monitor clinical
).
+
ESA
Соседние файлы в папке Библиотека им академика М.И. Перельмана