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Exam Review

Key Facts: CMN Nefrología Exam

16 Jan 2027

Exam date (in person, computer-administered)

CMN Fechas para certificación

300 items

Clinical-case items with serial questions

CMN Descripción del examen

1 Aug-31 Oct 2026

Document submission period

CMN Fechas para certificación

MXN 6,200

Certification fee

CMN Costos de certificación

CDMX & Guadalajara

Exam venues

CMN Descripción del examen

The CMN certification is the CONACEM-recognized board exam for nephrology in Mexico: 300 computer-administered clinical-case items on 16 January 2027 in Mexico City and Guadalajara. Documents are due 1 August-31 October 2026 and the fee is MXN 6,200.

Sample CMN Nefrología Practice Questions

Try these sample questions to review concepts for the CMN Nefrología exam. Each question includes a detailed explanation. Start the interactive quiz above for the full 104+ question experience with AI tutoring.

1A 28-year-old previously healthy woman presents with abrupt-onset generalized anasarca, periorbital edema, and foamy urine developing over 5 days. Laboratory evaluation reveals serum albumin of 1.8 g/dL, total cholesterol of 380 mg/dL, serum creatinine of 0.8 mg/dL, and a 24-hour urine protein of 9.2 g. Serological testing for ANA, anti-PLA2R, HIV, and hepatitis B/C is negative, and complement levels (C3, C4) are normal. What is the pathognomonic renal biopsy finding on electron microscopy, and what is the recommended first-line therapy?
A.Diffuse effacement of podocyte foot processes; oral prednisone at 1 mg/kg/day (maximum 80 mg/day)
B.Subepithelial electron-dense deposits with podocyte detachment; cyclical intravenous cyclophosphamide alternating with high-dose methylprednisolone
C.Subendothelial immune complex deposits; oral mycophenolate mofetil at 2 g/day combined with oral calcineurin inhibitors and low-dose steroids
D.Mesangial electron-dense deposits with IgA dominance; oral targeted-release formulation of budesonide at 16 mg daily for 9 months
Explanation: The clinical vignette describes adult minimal change disease (MCD), which accounts for 10% to 15% of nephrotic syndrome cases in adults. Light microscopy typically shows normal glomeruli, and immunofluorescence is negative. The pathognomonic finding on electron microscopy is diffuse effacement of visceral epithelial cell (podocyte) foot processes without immune complex deposition. The first-line therapy according to KDIGO guidelines is high-dose oral corticosteroids (prednisone 1 mg/kg/day or 2 mg/kg on alternate days, maximum 80 mg/day) for a minimum of 4 weeks up to 16 weeks to achieve complete remission.
2A 52-year-old man presents with bilateral lower extremity edema and nephrotic-range proteinuria (7.5 g/24 hours). His serum creatinine is 1.0 mg/dL and serum albumin is 2.2 g/dL. Circulating autoantibodies against the M-type phospholipase A2 receptor (anti-PLA2R) are detected at a high titer of 180 RU/mL by ELISA. Secondary workup for infection, systemic autoimmunity, and malignancy is entirely negative. According to KDIGO 2021 guidelines, what is the clinical role of anti-PLA2R antibodies in the diagnosis and disease monitoring of this patient?
A.They confirm secondary membranous nephropathy and indicate an urgent requirement for total body computed tomography and age-appropriate cancer screening to detect occult carcinoma.
B.High anti-PLA2R titers allow definitive non-invasive diagnosis in low-risk patients, and serial titers monitor immunological remission ahead of clinical proteinuria changes.
C.They represent non-specific acute-phase reactants that fluctuate with serum albumin concentration and should never be used to guide or withhold immunosuppressive therapy.
D.Their presence indicates rapidly progressive crescentic glomerulonephritis requiring immediate initiation of therapeutic plasma exchange and intravenous cyclophosphamide.
Explanation: Anti-PLA2R autoantibodies are present in 70% to 80% of patients with primary membranous nephropathy (pMN). Under KDIGO 2021 guidelines, a high-titer positive anti-PLA2R by ELISA in a nephrotic patient with preserved kidney function and no secondary features allows a confident non-invasive diagnosis of primary MN, avoiding kidney biopsy unless atypical features (unexplained eGFR decline, active urine sediment) exist. Immunologically, anti-PLA2R antibody levels decline or disappear weeks to months before clinical proteinuria resolves, making serial titers the primary tool for monitoring treatment response and disease relapse.
3A 44-year-old male with a BMI of 38 kg/m² and a 10-year history of hypertension is found to have asymptomatic proteinuria of 2.8 g/24 hours during an annual checkup. His serum albumin is 3.9 g/dL, serum creatinine is 1.3 mg/dL, and he has no peripheral edema. Renal biopsy demonstrates segmental sclerosis in 3 of 18 glomeruli, perihilar distribution of sclerosis, and significant glomerulomegaly. Electron microscopy shows focal, patchy foot process effacement covering 30% of the glomerular capillary surface. Which diagnosis and management strategy is most appropriate?
A.Primary FSGS due to circulating permeability factor; prompt initiation of oral prednisone at 1 mg/kg/day for 16 consecutive weeks
B.Collapsing glomerulopathy associated with occult viral infection; immediate pulse methylprednisolone and intravenous rituximab
C.Secondary FSGS due to hyperfiltration (obesity-related); supportive therapy with RAS inhibition, SGLT2 inhibition, and weight loss
D.Minimal change disease with focal sampling artifact; high-dose oral cyclosporine combined with low-dose alternate-day prednisone therapy for 12 months
Explanation: Secondary focal segmental glomerulosclerosis (FSGS) caused by hemodynamic hyperfiltration (such as in morbid obesity, reduced nephron mass, or chronic hypertension) characteristically presents with non-nephrotic or asymptomatic proteinuria, normal or near-normal serum albumin, absence of edema, perihilar glomerular sclerosis, glomerulomegaly, and patchy/focal foot process effacement on electron microscopy (<50% effacement). In contrast, primary FSGS is driven by a circulating permeability factor, presenting abruptly with full nephrotic syndrome (severe hypoalbuminemia, marked edema) and diffuse (>80%) foot process effacement. Secondary FSGS does NOT respond to immunosuppression and must be treated with hemodynamic nephroprotection (ACEi/ARB, SGLT2i) and weight loss.
4A 35-year-old man of West African descent presents with severe nephrotic syndrome, worsening renal function (serum creatinine increased from 1.1 to 3.4 mg/dL over 6 weeks), and heavy proteinuria of 14 g/24 hours. Renal biopsy reveals collapsing focal segmental glomerulosclerosis with marked podocyte hypertrophy and hyperplasia forming pseudocrescents. Genetic testing reveals homozygous APOL1 high-risk variants (G1/G1). What is the cellular mechanism by which APOL1 high-risk variants cause podocyte injury and collapsing glomerulopathy?
A.Mutated APOL1 protein accumulates extracellularly in the lamina densa of the GBM, displacing heparin sulfate proteoglycans and disrupting charge selectivity across the entire filtration barrier.
B.Variant APOL1 proteins act as circulating decoy receptors for vascular endothelial growth factor (VEGF), causing widespread capillary endothelial cell apoptosis and secondary microvascular thrombosis.
C.High-risk APOL1 alleles trigger autoantibody production against nephrin and podocin in the podocyte slit diaphragm.
D.Variant APOL1 proteins form cation-permeable channels in podocyte endolysosomal and plasma membranes, causing intracellular ion dysregulation, mitochondrial dysfunction, and podocyte necrosis.
Explanation: Apolipoprotein L1 (APOL1) G1 and G2 alleles evolved in sub-Saharan Africa as evolutionary protection against Trypanosoma brucei rhodesiense. When two risk alleles are inherited (G1/G1, G2/G2, or G1/G2), individuals have an elevated risk of developing focal segmental glomerulosclerosis (FSGS), especially the aggressive collapsing variant, and HIV-associated nephropathy (HIVAN). The pathophysiological mechanism involves intracellular APOL1 variant protein insertion into podocyte endolysosomal and plasma membranes, creating pH-sensitive cation-permeable pores that lead to potassium efflux, sodium/calcium influx, mitochondrial swelling, autophagic block, and podocyte lysis/necrosis.
5A 56-year-old woman with biopsy-proven primary membranous nephropathy has completed 6 months of optimized supportive therapy with maximally tolerated ramipril, dapagliflozin, and atorvastatin. At her 6-month evaluation, her 24-hour proteinuria remains 9.5 g, serum albumin is 2.1 g/dL, serum creatinine is 1.2 mg/dL (eGFR 53 mL/min/1.73 m²), and her anti-PLA2R titer is 240 RU/mL. According to KDIGO 2021 clinical practice guidelines, what is her risk category and the recommended first-line immunosuppressive therapy?
A.High risk of progressive kidney disease; rituximab (two 1,000 mg infusions separated by 14 days) or cyclical cyclophosphamide alternating with corticosteroids
B.Low risk of progressive kidney disease; continue conservative antiproteinuric therapy with RAS blockade and SGLT2 inhibition for an additional 12 months before considering any immunosuppressive regimen.
C.Moderate risk of progression; initiate monotherapy with high-dose oral prednisone at 1 mg/kg/day for 6 months while withholding targeted B-cell depleting agents or alkylators.
D.Very high risk of ESRD; immediate bilateral nephrectomy followed by emergent deceased-donor kidney transplantation
Explanation: Under KDIGO 2021 guidelines for membranous nephropathy, patients are stratified into low, moderate, high, or very high risk of CKD progression. High risk includes eGFR < 60 mL/min/1.73 m² and/or proteinuria > 8 g/day persisting for > 6 months, or proteinuria > 3.5 g/day that has not fallen by > 50% after 6 months of supportive therapy together with markers such as serum albumin < 2.5 g/dL or anti-PLA2R > 50 RU/mL. Very high risk is reserved for life-threatening nephrotic syndrome or rapid, otherwise unexplained loss of kidney function. This patient meets several high-risk criteria. In high-risk patients, wait-and-see conservative management is inappropriate. First-line therapy consists of rituximab (either 375 mg/m² weekly for 4 doses or 1,000 mg on days 1 and 15) or cyclical alkylating therapy (cyclophosphamide alternating monthly with corticosteroids for 6 months, the modified Ponticelli regimen).
6A 24-year-old male undergoes a percutaneous kidney biopsy for persistent microscopic hematuria, dysmorphic erythrocytes, and proteinuria of 1.6 g/24 hours following episodes of macroscopic hematuria coinciding with upper respiratory tract infections. Immunofluorescence confirms strong mesangial IgA and C3 deposition. The renal pathology report provides an Oxford Classification (MEST-C score) of M1, E1, S1, T0, C1. What do these individual MEST-C histological parameters represent?
A.Membranous basement spikes (M), Endothelial fenestration loss (E), Subendothelial dense deposits (S), Tubulointerstitial nephritis (T), and Crescentic necrosis (C)
B.Mesangial hypercellularity (M), Endocapillary hypercellularity (E), Segmental sclerosis (S), Tubular atrophy/fibrosis (T), and Crescents (C)
C.Microalbuminuria severity (M), Eosinophiluria percentage (E), Subepithelial dense humps (S), Thrombotic microangiopathy (T), and Complement consumption (C)
D.Macrophage interstitial infiltration (M), Epithelial shedding (E), Sclerotic nodular lesions (S), Transitional cell metaplasia (T), and Capsular synechiae (C)
Explanation: The Oxford Classification of IgA Nephropathy (updated in 2016 to the MEST-C score) identifies five independent histological lesions predictive of clinical outcome: M = Mesangial hypercellularity (M0 ≤50% of glomeruli, M1 >50%); E = Endocapillary hypercellularity (E0 absent, E1 present); S = Segmental glomerulosclerosis/adhesion (S0 absent, S1 present); T = Tubular atrophy and interstitial fibrosis (T0 ≤25%, T1 26%-50%, T2 >50%); and C = Cellular or fibrocellular crescents (C0 absent, C1 present in <25% of glomeruli, C2 present in ≥25%). The presence of E1 and C1 indicates active inflammatory lesions that may benefit from immunosuppressive intervention, whereas T reflects chronicity.
7A 32-year-old woman with biopsy-proven primary IgA nephropathy (Oxford M1, E0, S1, T1, C0) and baseline eGFR of 65 mL/min/1.73 m² has persistent proteinuria of 1.8 g/24 hours despite 6 months of maximally tolerated losartan (100 mg daily) and empagliflozin (10 mg daily). Her blood pressure is 118/74 mmHg. According to recent clinical trial evidence (NefIgArd trial) and updated KDIGO guidance, which targeted agent is designed to suppress mucosal production of galactose-deficient IgA1 (Gd-IgA1) in the distal ileum while minimizing systemic corticosteroid toxicity?
A.Intravenous cyclophosphamide pulse therapy (0.5 to 1.0 g/m² monthly) for 6 cycles combined with high-dose oral prednisone
B.Multi-target therapy combining oral mycophenolate sodium (1,440 mg daily) with low-dose oral tacrolimus (trough 3-5 ng/mL)
C.Targeted-release formulation of budesonide (TRF-budesonide, Nefecon) 16 mg once daily for 9 months
D.Eculizumab 900 mg weekly for terminal complement blockade combined with therapeutic plasma exchange
Explanation: Targeted-release formulation of budesonide (TRF-budesonide / Nefecon) is an enteric-coated formulation designed to deliver budesonide specifically to the mucosal Peyer's patches of the distal ileum, the primary site of origin of galactose-deficient IgA1 (Gd-IgA1) in IgA nephropathy. In the landmark phase 3 NefIgArd trial, 16 mg daily of TRF-budesonide for 9 months significantly reduced proteinuria and slowed eGFR decline over 2 years compared to placebo, with minimal systemic corticosteroid side effects due to extensive (>90%) first-pass hepatic metabolism.
8A 26-year-old woman with systemic lupus erythematosus (SLE) presents with facial rash, inflammatory polyarthritis, worsening hypertension (155/95 mmHg), lower extremity edema, and dark urine. Laboratory testing reveals serum creatinine of 1.9 mg/dL, serum albumin of 2.6 g/dL, 24-hour urine protein of 3.8 g, and active urine sediment containing RBC casts and dysmorphic red blood cells. Serum complement levels reveal C3 of 32 mg/dL (normal 90-180) and C4 of 6 mg/dL (normal 16-47), with high-titer anti-dsDNA antibodies (>400 IU/mL). Renal biopsy shows diffuse global endocapillary and extracapillary proliferation involving 75% of glomeruli with marked subendothelial immune deposits ('wire loops') and full-house immunofluorescence. What is the ISN/RPS classification of this lesion?
A.Class II: Mesangial proliferative lupus nephritis with isolated mesangial immune deposits
B.Class III: Focal proliferative lupus nephritis involving less than 50% of glomeruli with active necrotizing lesions
C.Class V: Membranous lupus nephritis presenting with nephrotic proteinuria and diffuse subepithelial deposits
D.Class IV: Diffuse proliferative lupus nephritis (≥50% glomeruli involved)
Explanation: According to the International Society of Nephrology / Renal Pathology Society (ISN/RPS) classification of lupus nephritis, Class IV represents Diffuse Proliferative Lupus Nephritis, defined by active or chronic endocapillary or extracapillary proliferation involving ≥50% of all glomeruli. It typically displays prominent subendothelial immune deposits producing classic 'wire loop' lesions on light microscopy, full-house immunofluorescence (IgG, IgA, IgM, C3, and C1q), severe hypocomplementemia, and high anti-dsDNA titers. It carries the highest risk of progression to end-stage kidney disease if not treated aggressively.
9A 29-year-old woman is diagnosed with biopsy-proven ISN/RPS Class IV lupus nephritis with a high activity index and preserved kidney function. According to the 2024 KDIGO Clinical Practice Guideline for the Management of Lupus Nephritis, which initial regimen has shown higher complete renal response rates than standard therapy while allowing reduced-dose glucocorticoids?
A.Add-on therapy: belimumab with MMF or low-dose IV cyclophosphamide, or a calcineurin inhibitor such as voclosporin with MMF, plus reduced-dose glucocorticoids
B.High-dose intravenous pulsed methotrexate (100 mg/m²) alternating with oral azathioprine (2 mg/kg/day) and high-dose oral dexamethasone pulses
C.Monotherapy with hydroxychloroquine 400 mg daily without any additional immunosuppressive agents, maintaining conservative management indefinitely
D.Immediate maintenance hemodialysis combined with therapeutic plasma exchange for 12 consecutive weeks without concurrent immunosuppressive drugs
Explanation: Recent landmark clinical trials (BLISS-LN for belimumab; AURORA 1 and 2 for voclosporin) demonstrated that adding either belimumab (a BLyS/BAFF inhibitor) or voclosporin (a novel calcineurin inhibitor) to background therapy of mycophenolate mofetil and reduced-dose glucocorticoids significantly increases complete renal response rates, reduces renal flare rates, and minimizes glucocorticoid exposure. The 2024 KDIGO guideline lists these add-on regimens (belimumab with MMF or low-dose cyclophosphamide; a calcineurin inhibitor with MMF when kidney function is not significantly impaired) alongside MMF or low-dose cyclophosphamide with glucocorticoids as recommended initial options for active Class III/IV lupus nephritis. The 2018 ISN/RPS revision replaced the old segmental/global and A/C labels with activity and chronicity indices.
10A 34-year-old woman with Class IV lupus nephritis achieves complete clinical remission after 6 months of induction therapy. She is now transitioning to long-term maintenance immunosuppression. According to the landmark Aspreva Lupus Management Study (ALMS maintenance phase), which agent is superior in terms of time to treatment failure and prevention of renal relapse?
A.Oral azathioprine administered at a target maintenance dose of 2.0 to 2.5 mg/kg/day
B.Mycophenolate mofetil (MMF, 1 to 2 g/day)
C.Oral cyclophosphamide administered at a continuous maintenance dose of 1.5 to 2.0 mg/kg/day
D.Oral cyclosporine administered at a target whole-blood trough level of 150 to 200 ng/mL
Explanation: In the ALMS maintenance trial (Dooley et al., NEJM 2011), patients who had responded to induction therapy were randomized to maintenance therapy with either mycophenolate mofetil (1 to 2 g/day) or azathioprine (2 mg/kg/day). MMF was significantly superior to azathioprine in maintaining renal remission, delaying time to treatment failure, and reducing the incidence of renal relapse, with a comparable safety profile. MMF is therefore the preferred first-line maintenance agent in lupus nephritis (unless pregnancy is planned, in which case azathioprine is substituted).

About the CMN Nefrología Exam

Independent study practice by OpenExamPrep for the certification exam of the Consejo Mexicano de Nefrología, A.C. (CMN), a CONACEM-recognized specialty council. The official exam has 300 clinical-case items and is given in Spanish. This bank is an independent English-language MCQ study adaptation organized around the CMN adult study guide, KDIGO guidelines and the Mexican hemodialysis standard NOM-003-SSA3-2010; it is not an official translation or simulation of the CMN exam.

Exam sponsor: Consejo Mexicano de Nefrología, A.C. (CMN). The requirements and fees below concern the certification or admission exam, separate from our free practice resources.

Assessment

The CMN certification exam is a single in-person, computer-administered test of 300 items in clinical-case format, with serial questions for each case and one correct answer per item; it may include unscored pilot items. The 2027 exam is on Saturday 16 January 2027 in Mexico City and Guadalajara, and candidates are told whether they passed at the end of the exam and by email. The CMN does not publish a time limit, pass mark or topic weights.

Time Limit

not-published

Passing Score

not-published

Exam / Certification Fees

MXN 6,200

Exam sponsor website

Fees, eligibility, and exam policies can change. Confirm them with the exam sponsor before applying or paying.

Official sources

Our practice resources: topics covered

We aim to reflect publicly available exam outlines and topic information in our study resources. Coverage, format, and difficulty may differ from the actual exam, and we cannot guarantee that every detail is accurate or current. Confirm exam requirements, fees, and policies with the official exam sponsor.

Weight not published

Glomerulopatías Primarias y Secundarias

Minimal change disease, focal segmental glomerulosclerosis (genetic, APOL1, primary vs secondary), membranous nephropathy (anti-PLA2R, anti-THSD7A), IgA nephropathy (Oxford MEST-C score), lupus nephritis (ISN/RPS classes I-VI), ANCA vasculitis, and anti-GBM disease

Weight not published

Lesión Renal Aguda, Trastornos Hidroelectrolíticos y Equilibrio Ácido-Base

KDIGO criteria for AKI, diagnostic urine indices (FENa, FEUrea), acute interstitial nephritis, obstructive uropathy, the kidney in pregnancy, cardiorenal and hepatorenal syndromes, hyponatremia and hypernatremia algorithms, dyskalemias, and high vs normal anion gap metabolic acidoses

Weight not published

Enfermedad Renal Crónica y Terapias de Reemplazo Renal

CKD staging (G1-G5, A1-A3), nephroprotective therapy (RASi, SGLT2i, finerenone, GLP-1 RA), CKD-MBD, anemia of CKD, hemodialysis adequacy (Kt/V) and vascular access, hemodialysis water quality and dialyzer reuse (NOM-003-SSA3-2010), peritoneal dialysis (PET test), and peritonitis

Weight not published

Trasplante Renal e Inmunología

HLA typing, PRA, donor-specific antibodies (DSA), crossmatching, induction/maintenance immunosuppression (thymoglobulin, tacrolimus, mycophenolate), cellular vs antibody-mediated rejection, BK virus nephropathy, and CMV prophylaxis

Weight not published

Nefropatías Tubulointersticiales, Hereditarias y Vasculares

Autosomal dominant polycystic kidney disease (Mayo imaging classification, tolvaptan), Alport syndrome, Fabry disease, kidney stones, complicated urinary tract infection, renal artery stenosis (FMD vs atherosclerosis), and thrombotic microangiopathies (aHUS vs TTP)

Preparing for the CMN Nefrología Exam

What You Need to Know

  • Passing score: not-published
  • Assessment: The CMN certification exam is a single in-person, computer-administered test of 300 items in clinical-case format, with serial questions for each case and one correct answer per item; it may include unscored pilot items. The 2027 exam is on Saturday 16 January 2027 in Mexico City and Guadalajara, and candidates are told whether they passed at the end of the exam and by email. The CMN does not publish a time limit, pass mark or topic weights.
  • Time limit: not-published
  • Exam / certification fees: MXN 6,200 Official sources

Using Our Practice Resources

  • Work through all 104 available questions
  • Review every answer and explanation
  • Track weak areas and revisit them
  • Use our AI tutor for tough concepts

CMN Nefrología: Suggested Study Strategy

1Master the KDIGO glomerulopathy algorithms: indications for anti-PLA2R titration in membranous nephropathy, targeted budesonide and SGLT2i in IgA nephropathy, and multimodal induction (voclosporin or belimumab + MMF/steroids) in proliferative lupus nephritis.
2Rehearse urinary indices and diagnostic formulas: fractional excretion of sodium (FENa) vs urea (FEUrea) in patients on loop diuretics, transtubular potassium gradient (TTKG), and winter's formula for respiratory compensation in metabolic acidosis.
3Know dialysis adequacy benchmarks and Mexican rules: spKt/V minimum 1.2 (target 1.4) for thrice-weekly hemodialysis, total weekly Kt/V of about 1.7 in peritoneal dialysis, NOM-003-SSA3-2010 dialyzer reuse limits (12 reuses, residual volume at least 80%, no reuse with HBV or HIV), ISO water limits (100 CFU/mL, 0.25 EU/mL), and empirical intraperitoneal antibiotics for PD peritonitis.
4Review renal transplant immunology thoroughly: differentiate T-cell mediated rejection (tubulitis, interstitial inflammation) from antibody-mediated rejection (C4d deposition, microvascular inflammation, DSA), and understand BK polyomavirus management.
5Focus on recent cardiorenal and nephroprotective trials: indications and eGFR cutoffs for SGLT2 inhibitors, non-steroidal mineralocorticoid receptor antagonists (finerenone), and GLP-1 receptor agonists in diabetic and non-diabetic CKD.
6Work through the full CMN study guide, including stones, obstruction, urinary infection and the kidney in pregnancy, not only glomerular disease and dialysis.

Frequently Asked Questions

What is the Consejo Mexicano de Nefrología (CMN) certification exam?

It is the board certification exam of the Consejo Mexicano de Nefrología, A.C., one of the specialty councils recognized by CONACEM. Nephrologists who complete residency apply with their documents on the CMN platform and sit a single written exam; there are separate adult and pediatric nephrology tracks.

What is the format and schedule of the 2027 exam?

The exam has 300 items in clinical-case format, with serial questions per case and one correct answer each, and may include unscored pilot items. It is computer-administered in person on Saturday 16 January 2027 in Mexico City and Guadalajara. The convocatoria was published on 1 August 2026, documents are accepted from 1 August to 31 October 2026, acceptance is notified on 1 December 2026, and results are given at the end of the exam and by email.

How much does it cost, and what is the pass mark?

The CMN lists a certification fee of MXN 6,200, paid by bank deposit or transfer. The council does not publish a pass mark or time limit.

What does the exam cover?

The CMN adult study guide lists 25 topics, from renal structure, hormones and pharmacology through acute kidney injury, CKD, diabetic nephropathy, glomerular, tubulointerstitial, cystic, vascular, hereditary and toxic kidney disease, obstruction, stones, urinary infection, pregnancy, hemodialysis, peritoneal dialysis, transplantation, nutrition, hypertension, and fluid-electrolyte and acid-base disorders. No topic weights are published.

Why is this practice bank in English?

The CMN exam is given in Spanish. This OpenExamPrep bank is an independent English-language MCQ study adaptation for reviewing the clinical content; it is not an official translation or simulation of the CMN exam.