LAPORAN KASUS

Renal Tubular Acidosis

Abdullah
Identitas
 Ny. D
 34 tahun
 Alamat : ule kareng
 Pembiayaan: JKA
 Agama: Islam
 No RM:

 Keluhan utama: Lemas kadang-

kadang masih dirasakan (Ps kontrol
pasca perawatan)
 Januari 2011 2 4 Januari 2013

 Sering lemas  3 hari SMRS lemas

 Trauma, kelemahan  Sempat ke RS Ktk,
sesisi (-), diare (-) pp
 BAK normal, nyeri  Lemas (+)
pinggang (-)  Lemas kedua
 Dikatakan sakit ginjal tungkai  tdk bs
dengan banyak jalan (-) mual (+)
batu th 2009 muntah (-), diare (-)
 Dirawat hingga 11  Sesak (+)
kali dalam 2 tahun  BAK 3-4 kali/hari
 Minum KSR/Aspar K  dirawat di PW A 10
3x1 hari
 Riwayat penyakit dahulu
DM (-) asma (-) alergi obat(-) jantung (-)
kuning (-) ginjal (-)

 Riwayat penyakit keluarga

Ht (-) DM (-) Jantung (-) Asma (-) alergi
obat (-) penyakit ≈ pasien (-) ginjal (-)

 Riwayat sosial ekonomi

Riwayat minum obat lama (-)
Status: menikah, 3 anak sehat
Pembiayaan SKTM
Pemeriksaan fisik

 CM TSR
 TD 130/80 mmHg
 FN: 84 x/menit, reguler isi cukup, equal
 RR: 20 x/menit, teratur, dalam cukup
 S: 36,7 °C
 BB: 50 kg
 TB: 155 cm
 IMT 20,83
 Rambut : hitam tidak mudah dicabut
 Mata: konjungtiva pucat (+/+) sklera ikterik (-)
 Mulut: tonsil T1-T1, faring hiperemis-
 Leher JVP 5-2 cm H2O, tiroid tidak membesar
 KGB: submandibula, sternokleido, supraklavikula,
aksila tidak teraba
 Dada : simetris statis dan dinamis
 Jantung: I-II normal murmur (-) gallop (-)
 Paru : vesikuler, ronki -/- wh -/-
 Abdomen: datar, lemas, hepar dan limpa tidak
teraba, timpani, shifting dullness (-) BU (+) N
 Ekstremitas : akral hangat, edema -/-
 Motorik 5555/5555
5555/5555
 Pemeriksaan Laboratorium
Tgl 22/2/13 (IGD) 26/22/13 3/3/13 KONTROL

Hb/Leu/Tr 9.9/14800/553000 9.1/10700/533000

MCV/CH 84/28
Alb/glob 3.31/2.9
SGOT/ 12
GDS 129 117
Ur/cr 22/1.4 CCT hit 42 ml/mnt
Na/k/Cl 146/2.1/121 139/3.23/116 141/3.35/1 141/2.62
17 /110
AGD: pH/pCO2 PO2 7.288/22.6/142/10 7.305/30/103/1 7.27/30/1
/ HCO3/SO2
.5/98 7/98 20/14/98
AG = 14.5 AG = 6 AG = 10
Ca serum 7.2 mg/dl 7.8
Fosfat serum 1.8 mg/dl
Mg 1.65 mg/dl
Asam urat 3.4 mg/dl
Pemeriksaan Serum Nilai Normal Urin Nilai Normal

Elektrolit
Na 142 135-145 mmol/l 284 30-220 mmol/24j
K 3.73 3,5-4,5 mmol/l 85 25-100 mmol/24j
Cl 120 97-107 mmol/l 301 120-250
1,7-2,5 mmol/l mmol/24j

Osmolality - 285-295 mOsm/kg - 250-900 mOs/kg

CCT ukur: 48.82
ml/mnt
Prot.Kuant: 840
mg/24 jam
Urinalisis: Leuko 30-45, eri 5-10/LPB,
BJ 1020, pH 7
Prot trace, darah 1+, LE 3+,
USG Ginjal 02/03-2013

Gambaran kelainan parenkim ginjal kronik bilateral

Nefrolitiasis Bilateral
 Ps wanita, 34 tahun dengan keluhan sering
lemas, intake normal, diare (-), BAK normal
riw.obat lama (-), didiagnosis nefrolitiasis multipel
sejak 1 th, normotensi, konjungtiva pucat,
Laboratorium menunjukkan anemia normositik
normokrom, hipokalemia, asidosis metabolik,
hiperkloremik, normal anion gap, hipoalbumin
ringan, CCT hitung 42 ml/mnt , peningkatan
ekskresi kalium urin, piuria, hematuria
USG parenkim ginjal kronik bilateral dan
nefrolitiasis Bilateral
Daftar masalah

1. Hipokalemia berulang
2. CKD stage III
3. Anemia normositik normokrom
4. Nefrolitiasis bilateral dengan hematuria
mikroskopik + piuria
5. Hipoalbuminemia ringan
Hipokalemia berulang

 a/d lemas berulang, intake normal,

riw.obat lama (-), hipokalemia berulang,
asidosis metabolik, hiperkloremik, ekskresi
kalium urin 85 meq/hari
 Dipikirkan hipokalemia berulang ec RTA
tipe I (distal)
kalium urin 85 meq
Harrison’s Principles of Internal
Medicine. Ed 17. McGrawHill, New
York, 2008. P. 282-5
Hipokalemia
Terapi
• Indikasi mutlak – segera:
- Sedang dalam pengobatan digitalis
- KAD
- Kelemahan otot pernapasan
- Hipokalemia berat (K < 2meq/L)
• Indikasi kuat
- Insufisiensi koroner / iskemi miokard
- Ensefalopati hepatikum
- Konsumsi obat  perpindahan K
• Indikasi sedang
- Hipokalemia ringan

Oral  lebih disenangi

- 40-60 meq  ↑ 1-1,5 meq/L
- 135-160 meq  ↑ 2,5-3,5 meq/L

[K+]CCD = [K+]U : (OSMU/OSMP) Intravena (KCl)

TTKG = [K+]CCD = [K+]U : (OSMU/OSMP) - Vena besar, 10-20 meq/jam
[K+]P [K+]P - Aritmia / kelumpuhan otot napas  40-100 meq/jam
- KCl max 60 meq dalam NaCl isotonik 1000 ml
Renal Tubular Acidosis
 Group of transport defects produced by a failure to
reabsorb filtered bicarbonate (type II), or an inability
to excrete the daily endogenous metabolic acid
load (type I).
 Renal tubular acidosis (RTA) syndromes are
characterized by a normal anion gap metabolic
acidosis, hyperchloremia, and relatively normal renal
function.
 Distal RTA (type I):
› Produced by an impaired distal acidification and
characterized by an inability to lower urinary pH
maximally (<5.5) under systemic acidemia
› The main defect is an inability to secrete hydrogen ions
or a back-leak of secreted hydrogen ions in the
collecting duct.
Renal Tubular Acidosis - lab
 Serum electrolytes test:
› Helps to identify the presence of normal
anion gap (8–16 mEq/L), metabolic
acidosis, hypokalemia, or hyperkalemia
INVESTIGATIONS DISTAL RTA:
1. Serum
 normal anion gap
hyperchloremic metabolic
acidosis (with low serum HCO3)
 hypokalemia, hyponatremia,
hypophosphatemia
 normal or slightly elevated
calcium
 normal or slightly elevated
phosphate
 normal or decreased glomerular
filtration rate (GFR)
 elevated parathyroid hormone
2. Urine
pH >5.5 (usually between 6-7)
hypercalciuria
aminoaciduria (with severe bone
disease)
bicarbonaturia
tubular proteinuria
leukocyturia
elevated rate of excretion of
phosphate, calcium, and potassium
decreased rate of excretion of citrate,
ammonium, titratable acid
 Serum creatinine: Helps to exclude renal failure
 Urine anion gap and urine pH:
› If urine pH is <6.0, then type I RTA can be ruled out.
› Negative urine anion gap (Cl > Na + K) is seen in GI losses and
proximal RTA.
› Positive urine anion gap is seen in distal RTA.
 Urine spot for calcium/creatinine ratio: Patients with RTA can have
hypercalciuria.
 Tubular reabsorption of phosphate (TRP): TRP <60% can be seen in
Fanconi syndrome and other causes of proximal RTA. Aminoaciduria
can also be present.
 24-hour urine for citrate, calcium, potassium, and oxalate:
Hypercalciuria and hypocitraturia are risk factors for nephrocalcinosis
and/or Nephrolithiasis.
Tthe pathophysiologic mechanism(s)
 1. Secretory Defect
 failure of the collecting ducts to secrete hydrogen ion due to:
› decreased number or impaired function of hydrogen ion secretory pumps
› structural defects in the luminal membrane of the collecting ducts
› an impaired energy supply
 results in an inability to reduce the urine pH to less than 5.5
 2. Voltage Dependent Defect
 inability of distal nephrons to generate and/or maintain a negative
intratubular potential difference due:
› a defect in sodium delivery and/or transport -> persistent distal defect in
sodium reabsorption
 would reduce secretion of both hydrogen ions & K+
 3. Gradient Defect
 increased permeability of the luminal membrane to H+, carbonic acid, or
bicarbonate
RDx/: Cek AGD dan e ulang
RTh/:
 KSR 3 x 1 tab
 Diet buah (pisang 3 buah/hari)
 Bicnat 3x1
 Edukasi
Medical Management
 1. Oral Alkali Supplements
 potassium citrate
› may relieve hypocitraturia
› may decrease rate of stone formation
 sodium or potassium bicarbonate
 corrects metabolic acidosis
 maintains normal rate of calcium excretion
 lifelong therapy and attempts to withdraw results in the
reappearance of metabolic acidosis and related
symptoms - may halt progression of nephrocalcinosis
and growth retard-ation but not polyuria
 2. Potassium Supplements
Renal Tubular Acidosis - FOLLOW UP
 Patients with RTA should be closely monitored with
frequent potassium and plasma bicarbonate levels until a
steady state is reached.
 Untreated type I RTA can lead to renal failure by causing
progressive nephrocalcinosis, adequate alkali therapy is
usually enough to avoid this complication.
 Patients with hypercalciuria should be monitored with spot
urine calcium/creatinine ratio.
 Renal ultrasound follow-up is recommended in patients
with nephrocalcinosis.
 Avoid hemolyzed specimens that may
artificially increase the serum potassium and
reduce the plasma bicarbonate levels.
 Administer alkali over several divided doses.
 Closely monitor patients during episodes of
gastroenteritis to avoid dehydration and severe
metabolic acidosis.
 Atas dasar, CCT 48, USG parenkim ginjal
kronik
 Rdx: calsium, fosfat, ur, cr serial
 Rth/: edukasi
 AF/B12/CaCO3/Bicnat
 Protein 0.6-0.75 g/kgBB/hari
Nefrolitiasis bilateral dengan piuria
dan hematuria

 a/d didiagnosis batu ginjal 1t tahun, hematuria,

piuria, hasil USG nefrolitiasis bilateral, RTA tipe 1
 Dipikirkan nefrolitiasis ec komplikasi RTA tipe 1
 Rencana:
- Pengukuran citrate dan calcium urin 24 jam, kultur urin, analisis
urin ulang
konsul urologi (ulang)
 An important complication of chronic renal tubular acidosis
(mainly distal, type I) is nephrocalcinosis and urolithiasis. A
number of pathophysiological alterations contribute to stone
formation:
 Buffering of the chronic acid load by the bone, causing bone
dissolution and promoting hypercalciuria
 Diminution of renal tubular calcium reabsorption, further
aggravating the hypercalciuria
 Hypocitraturia because of avid citrate reabsorption by the
proximal tubule
 High urinary pH, causing insolubility of calcium phosphate
and promoting its precipitation www.medscape.com
Hypocitraturia
 Hypocitraturic calcium nephrolithiasis may exist as an isolated abnormality
(10%) or more commonly in combination with other metabolic disorders
(50%).
 Acid-base status, acidosis in particular, is the most important factor affecting
the renal handling of citrate, with increased acid levels resulting in
diminished endogenous citrate production.
 Low urinary citrate causes the urinary environment to become
supersaturated with calcium salts, promoting nucleation, growth, and
aggregation, resulting in stone formation.
› A more common cause of hypocitraturia is distal RTA
› Acidosis impairs urinary citrate excretion by enhancing renal tubular
reabsorption of citrate as well as by reducing its synthesis.
› Distal RTA can be complete or incomplete. In both forms, hypercalciuria
and profound hypocitraturia may be associated. In combination with
alkaline urine, the patient is at risk for developing calcium oxalate or
calcium phosphate stones
www.medscape.com
INVESTIGATIONS DISTAL RTA:
1. Serum
 normal anion gap
hyperchloremic metabolic
acidosis (with low serum HCO3)
 hypokalemia, hyponatremia,
hypophosphatemia
 normal or slightly elevated
calcium
 normal or slightly elevated
phosphate
 normal or decreased glomerular
filtration rate (GFR)
 elevated parathyroid hormone
2. Urine
pH >5.5 (usually between 6-7)
hypercalciuria
aminoaciduria (with severe bone
disease)
bicarbonaturia
tubular proteinuria
leukocyturia
elevated rate of excretion of
phosphate, calcium, and potassium
decreased rate of excretion of citrate,
ammonium, titratable acid
 Atas dasar
› Riwayat lemas, sakit ginjal 1 tahun, perdarahan
(-)
› Hb 9 normositik normokrom
Dipikirkan anemia renal dd/ occult bleeding
Rdx: morfologi eritrosit, retikulosit, feritin, saturasi
transferin, serum iron
Rth/ jika perdarahan (-), feritin normal  EPO
 Atas dasar albumin 3.3 mg/dl
 Proteinuria : trace
 Dipikirkan hipoalbuminemia ringan ec
renal loss
 Rdx: protein kuantitatif urin/24 jam
 Th/: Protein 0.6-0.75 g/kgbb/hari
- atasi penyebab
 Pasien dengan RTA klasik tipe I, CKD
stage III, nefrolitiasis bilateral dengan
hematuria mikroskopis dan piuria,
anemia dan hipoalbumin ringan, kontrol
ke poliklinik nefrologi dengan
hipokalemia berulang
TATA LAKSANA SELANJUTNYA?
Terima Kasih
•TTKG: ratio of [K+] in the lumen of the cortical
collecting duct ([K+]CCD ) to that in peritubular
capillaries or plasma ([K+]P )
•Formula:
TTKG= K+ urine/K+ plasma 
OSMU /OSMP
 DISTAL RENAL TUBULAR ACIDOSIS
 DEFINITION:
 A renal disorder characterized by the inability of the
collecting duct to decrease the urinary pH below 5.5
resulting in an excessive urinary loss of bicarbonate.
 EPIDEMIOLOGY:
 incidence: ?
 age of onset:
› first year of life with failure to thrive
PATHOGENESIS:
 1. Etiology
 Distal Renal Tubular Acidosis (RTA) represents the uniform response of the
distal renal tubules to various exogenous and endogenous insults that spare
the glomeruli but result in a generalized pattern of tubular dysfunction
 types of insults:
 1. Primary
 1. Permanent
 1. Classic Form 2. Variants 1. Incomplete 2. With Nerve Deafness 2.
Transient
 1. Infantile Form 2. Secondary
 1. Conditions Associated with Nephrocalcinosis
 1. Hypomagnesemia-hypercalciuria with nephrocalcinosis 2. Hypercalcemic
Hyperthyroidism 3. Idiopathic Hypercalciuria with Nephrocalcinosis 4.
Primary Hyperparathyroidism 5. Vitamin D intoxication 2.
 3. Imaging Studies
 1. Renal (Ultrasound/CT/X-Rays)
 nephrocalcinosis (may appear within the 1st few months of life)
 nephrolithiasis, urolithiasis
 2. Musculoskeletal
 rickets, osteomalacia
 4. Pathology
 1. Kidney
 early - normal
 late - complications
› nephrocalcinosis
› chronic interstitial nephritis
 cellular infiltration, tubular atrophy, glomerular sclerosis
Gangguan Keseimbangan Kalium

 Kalium memasuki ICF

› ↑ [K+] plasma (intake), pelepasan insulin
ECF
 Ekskresi
3,5-5,5 meq/L
› Renal  rute utama
› ± 90% direabsorpsi di renal
› Sekresi  aldosteron dan hiperkalemia
 [K+] plasma normal: 3,5-5,5 mmol/L
 Fungsi normal neuromuskular K+
 Hipokalemia : [K+] < 3,5 mEq/L
 Hiperkalemia : [K+] > 5,5 mEq/L
120-160 meq/L
ICF
Hipokalemia
Terapi
• Indikasi mutlak – segera:
- Sedang dalam pengobatan digitalis
- KAD
- Kelemahan otot pernapasan
- Hipokalemia berat (K < 2meq/L)
• Indikasi kuat
- Insufisiensi koroner / iskemi miokard
- Ensefalopati hepatikum
- Konsumsi obat  perpindahan K
• Indikasi sedang
- Hipokalemia ringan

Oral  lebih disenangi

- 40-60 meq  ↑ 1-1,5 meq/L
- 135-160 meq  ↑ 2,5-3,5 meq/L

[K+]CCD = [K+]U : (OSMU/OSMP) Intravena (KCl)

TTKG = [K+]CCD = [K+]U : (OSMU/OSMP) - Vena besar, 10-20 meq/jam
[K+]P [K+]P - Aritmia / kelumpuhan otot napas  40-100 meq/jam
- KCl max 60 meq dalam NaCl isotonik 1000 ml