Kidney transplant pathology US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Kidney transplant pathology. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Kidney transplant pathology US Medical PG Question 1: A 48-year-old Caucasian male suffering from ischemic heart disease is placed on a heart transplant list. Months later, he receives a heart from a matched donor. During an endomyocardial biopsy performed 3 weeks later, there is damage consistent with acute graft rejection. What is most likely evident on the endomyocardial biopsy?
- A. Granuloma
- B. Atherosclerosis
- C. Lymphocytic infiltrate (Correct Answer)
- D. Tissue necrosis
- E. Fibrosis
Kidney transplant pathology Explanation: ***Lymphocytic infiltrate***
- Acute graft rejection, especially within weeks of transplantation, is characterized by a **cellular immune response** dominated by **T lymphocytes** invading the allograft.
- These lymphocytes target donor major histocompatibility complex (MHC) molecules, leading to myocyte damage and dysfunction, which would be visible as a lymphocytic infiltrate on biopsy.
*Granuloma*
- Granulomas are aggregates of **macrophages**, often seen in chronic inflammatory conditions like tuberculosis, sarcoidosis, or fungal infections.
- They are not typical findings in the context of acute allograft rejection.
*Atherosclerosis*
- Atherosclerosis is a disease of large and medium-sized arteries characterized by **plaque formation**, primarily involving lipid deposition and inflammation, which narrows the arterial lumen.
- While it can affect transplanted organs (e.g., transplant vasculopathy, a form of chronic rejection), it is not the primary mechanism or histological finding in **acute cellular rejection** occurring three weeks post-transplant.
*Tissue necrosis*
- While acute rejection can *lead* to tissue necrosis due to severe inflammation and ischemia, necrosis alone is a broad term and not the most specific or defining histological feature of acute cellular rejection.
- The preceding and primary histopathological hallmark of acute cellular rejection is the **inflammatory cell infiltrate**, particularly lymphocytes attacking the graft.
*Fibrosis*
- Fibrosis, or the deposition of excess connective tissue, is a characteristic feature of **chronic rejection** or chronic injury processes.
- It indicates long-standing damage and repair, which is unlikely to be the predominant finding in a biopsy three weeks after transplantation indicative of acute rejection.
Kidney transplant pathology US Medical PG Question 2: A 31-year-old female receives a kidney transplant for autosomal dominant polycystic kidney disease (ADPKD). Three weeks later, the patient experiences acute, T-cell mediated rejection of the allograft and is given sirolimus. Which of the following are side effects of this medication?
- A. Nephrotoxicity, hypertension
- B. Hyperlipidemia, thrombocytopenia (Correct Answer)
- C. Nephrotoxicity, gingival hyperplasia
- D. Pancreatitis
- E. Cytokine release syndrome, hypersensitivity reaction
Kidney transplant pathology Explanation: ***Hyperlipidemia, thrombocytopenia***
- **Sirolimus** (rapamycin) is an **mTOR inhibitor** commonly used in transplant immunology, which frequently causes **hyperlipidemia** (elevated cholesterol and triglycerides) and **thrombocytopenia** (low platelet count).
- Other common side effects include **myelosuppression** (leukopenia, anemia), **mouth ulcers**, and **impaired wound healing**.
*Nephrotoxicity, hypertension*
- **Nephrotoxicity** and **hypertension** are more characteristic side effects of **calcineurin inhibitors** like **tacrolimus** and **cyclosporine**, which are also used in transplant immunosuppression but have a different mechanism of action than sirolimus.
- While sirolimus can indirectly affect kidney function, it is generally considered less nephrotoxic than calcineurin inhibitors.
*Nephrotoxicity, gingival hyperplasia*
- **Gingival hyperplasia** is a hallmark side effect of **cyclosporine**, a calcineurin inhibitor, along with **hirsutism** and **nephrotoxicity**.
- Sirolimus does not typically cause gingival hyperplasia.
*Pancreatitis*
- While some immunosuppressants can rarely cause pancreatitis, it is not a common or characteristic side effect of **sirolimus**.
- **Azathioprine** is more frequently associated with pancreatitis among immunosuppressive agents.
*Cytokine release syndrome, hypersensitivity reaction*
- **Cytokine release syndrome** and acute **hypersensitivity reactions** are more often associated with **monoclonal antibodies** (e.g., **basiliximab**, **daclizumab**) used for induction therapy or treatment of acute rejection, particularly within hours or days of administration.
- Sirolimus is less likely to cause these immediate severe reactions.
Kidney transplant pathology US Medical PG Question 3: A 10-year-old boy is presented to the hospital for a kidney transplant. In the operating room, the surgeon connects an allograft kidney renal artery to the aorta, and after a few moments, the kidney becomes cyanotic, edematous, and dusky with mottling. Which of the following in the recipient’s serum is responsible for this rejection?
- A. Macrophages
- B. CD4+ T cells
- C. IgA
- D. CD8+ T cells
- E. IgG (Correct Answer)
Kidney transplant pathology Explanation: ***IgG***
- The rapid onset of tissue necrosis and the immediate signs of rejection (cyanotic, edematous, dusky with mottling) upon vascular anastomosis are characteristic of **hyperacute rejection**.
- **Hyperacute rejection** is mediated by pre-formed recipient antibodies, primarily **IgG**, targeting donor ABO or HLA antigens. These antibodies activate complement, leading to rapid thrombosis and graft destruction.
*Macrophages*
- While macrophages play a role in chronic allograft rejection and delayed type hypersensitivity, they are not the primary mediators of **hyperacute rejection**.
- Their involvement typically presents with a more delayed and less immediate profound tissue damage than seen in this scenario.
*CD4+ T cells*
- **CD4+ T cells** are central to acute cellular rejection, which typically manifests days to weeks after transplantation.
- They are not responsible for the immediate, pre-formed antibody-mediated response seen in **hyperacute rejection**.
*IgA*
- **IgA antibodies** are primarily involved in mucosal immunity and are generally not implicated in solid organ transplant rejection, especially hyperacute rejection.
- While IgA can contribute to immune complex formation, it's not the main antibody type driving hyperacute allograft destruction.
*CD8+ T cells*
- **CD8+ T cells** (cytotoxic T lymphocytes) are key players in acute cellular rejection, mediating direct lysis of donor cells.
- Their action is part of a cellular immune response that takes days to weeks to develop and is not responsible for the immediate, antibody-mediated hyperacute rejection.
Kidney transplant pathology US Medical PG Question 4: A 62-year-old female with a history of uncontrolled hypertension undergoes kidney transplantation. One month following surgery she has elevated serum blood urea nitrogen and creatinine and the patient complains of fever and arthralgia. Her medications include tacrolimus and prednisone. If the patient were experiencing acute, cell-mediated rejection, which of the following would you most expect to see upon biopsy of the transplanted kidney?
- A. Granular immunofluorescence around the glomerular basement membrane
- B. Lymphocytic infiltrate of the tubules and interstitium (Correct Answer)
- C. Crescent formation in Bowman’s space
- D. Drug precipitation in the renal tubules
- E. Sloughing of proximal tubular epithelial cells
Kidney transplant pathology Explanation: ***Lymphocytic infiltrate of the tubules and interstitium***
- **Acute cell-mediated rejection** is primarily characterized by the infiltration of **T lymphocytes** and macrophages into the allograft, leading to inflammation and damage.
- This cellular infiltrate is typically observed in the **interstitium and tubules** of the transplanted kidney.
*Granular immunofluorescence around the glomerular basement membrane*
- This finding is characteristic of **immune complex-mediated glomerulonephritis**, such as post-streptococcal glomerulonephritis, and signifies deposition of immune complexes.
- It is not typical of acute cell-mediated rejection, which is driven by T-cells rather than circulating immune complexes.
*Crescent formation in Bowman’s space*
- **Crescents** in Bowman's space are indicative of rapidly progressive glomerulonephritis (RPGN), a severe form of glomerular inflammation usually associated with conditions like Goodpasture syndrome or ANCA-associated vasculitis.
- While crescentic glomerulonephritis can cause acute kidney injury, it is not the primary histological hallmark of acute cell-mediated transplant rejection.
*Drug precipitation in the renal tubules*
- **Drug precipitation** can occur with certain medications, leading to acute kidney injury (e.g., sulfonamides, methotrexate), but it is a chemical injury, not an immune-mediated rejection process.
- The patient's symptoms of fever and arthralgia, along with elevated creatinine, point towards an inflammatory immune response rather than drug toxicity alone.
*Sloughing of proximal tubular epithelial cells*
- **Sloughing of proximal tubular epithelial cells** is a hallmark of **acute tubular necrosis (ATN)**, often caused by ischemia or nephrotoxic agents.
- While ATN can also lead to elevated creatinine, the presence of fever and arthralgia, plus the context of transplantation, makes acute cell-mediated rejection a more likely diagnosis.
Kidney transplant pathology US Medical PG Question 5: A 50-year-old man presents to a clinic with oliguria. Four weeks ago, he had a kidney transplant. Postoperative follow-up was normal. He is currently on cyclosporine and admits that sometimes he forgets to take his medication. On physical examination, the vital signs include: temperature 37.1°C (98.8°F), blood pressure 165/110 mm Hg, heart rate 80/min, and respiratory rate 16/min. There is mild tenderness on renal palpation. His serum creatinine level is 4 mg/dL, well above his baseline level after the transplant. Which of the following best describes the histological finding if a biopsy is taken from the transplanted kidney?
- A. Lymphocytic infiltration of graft vessels and endothelial damage (Correct Answer)
- B. Thrombosis and occlusion of vessels
- C. Atherosclerosis on angiography
- D. Necrosis with granulation tissue
- E. Thickening of blood vessels, fibrosis of graft vessels, and parenchymal atrophy
Kidney transplant pathology Explanation: ***Lymphocytic infiltration of graft vessels and endothelial damage***
- The patient's presentation with **oliguria**, elevated **creatinine**, and **hypertension** following a recent kidney transplant, especially with a history of non-adherence to **cyclosporine** (an immunosuppressant), strongly indicates **acute rejection**.
- Histologically, acute rejection is characterized by **lymphocytic infiltration** of the graft vessels (often referred to as **vasculitis** or **endotheliitis**) and associated **endothelial damage**.
*Thrombosis and occlusion of vessels*
- This finding is more characteristic of **hyperacute rejection**, which typically occurs within minutes to hours of transplantation, not weeks later.
- Hyperacute rejection is mediated by **pre-formed antibodies** and leads to severe, rapid graft failure due to widespread intravascular thrombosis.
*Atherosclerosis on angiography*
- While post-transplant patients can develop accelerated atherosclerosis (a form of **chronic rejection**), it is typically a long-term complication developing months to years after transplantation.
- The acute presentation with rapid creatinine elevation is not typical for primary atherosclerosis.
*Necrosis with granulation tissue*
- **Necrosis** with **granulation tissue** is a general healing response to significant tissue injury or inflammation.
- While some cellular necrosis can occur in severe rejection, it's not the defining feature, and granulation tissue indicates a more prolonged, subacute process rather than the primary histological hallmark of acute rejection.
*Thickening of blood vessels, fibrosis of graft vessels, and parenchymal atrophy*
- These are classic features of **chronic rejection**, which manifests months to years after transplantation as a gradual decline in graft function.
- **Chronic rejection** involves progressive damage leading to vasculopathy, interstitial fibrosis, and tubular atrophy, rather than the acute inflammatory cellular infiltrate seen here.
Kidney transplant pathology US Medical PG Question 6: A 29-year-old woman comes to the physician because of a 2-day history of intermittent dark urine and mild flank pain. She has also had a cough, sore throat, and runny nose for the past 5 days. She has not had dysuria. She takes no medications. She has no known allergies. Her temperature is 37°C (98.6°F). Examination of the back shows no costovertebral angle tenderness. Laboratory studies show:
Hemoglobin 10.4 g/dL
Leukocyte count 8,000/mm3
Platelet count 200,000/mm3
Serum
Na+ 135 mEq/L
K+ 4.9 mEq/L
Cl- 101 mEq/L
HCO3- 22 mEq/L
Urea nitrogen 18 mg/dL
Creatinine 1.1 mg/dL
Urine
Color yellow
Blood 3+
Protein 1+
Leukocyte esterase negative
An ultrasound of the kidney and bladder shows no abnormalities. Which of the following is the most likely cause of this patient's symptoms?
- A. Ischemic tubular injury
- B. Urothelial neoplasia
- C. Renal papillary necrosis
- D. Renal glomerular damage (Correct Answer)
- E. Interstitial renal inflammation
Kidney transplant pathology Explanation: ***Renal glomerular damage***
- The patient's symptoms (dark urine, mild flank pain) occurring shortly after an **upper respiratory infection** (cough, sore throat, runny nose) are highly suggestive of **acute glomerulonephritis**.
- The urinalysis showing **hematuria (blood 3+) and proteinuria (protein 1+)** in the absence of dysuria or bacterial infection (leukocyte esterase negative, no CVA tenderness) points to glomerular inflammation as the cause of kidney involvement.
*Ischemic tubular injury*
- This condition typically presents with signs of **acute kidney injury**, such as elevated creatinine and blood urea nitrogen (BUN), which are not significantly altered here.
- Urinalysis usually shows **muddy brown casts** and signs of tubular damage, rather than prominent hematuria and proteinuria alone.
*Urothelial neoplasia*
- While it can cause painless hematuria, it is less likely to present with concurrent **flu-like symptoms** and the rapid onset described.
- Urothelial neoplasms are more common in older individuals or those with specific risk factors (e.g., smoking), and an **ultrasound revealed no abnormalities**.
*Renal papillary necrosis*
- This is typically seen in patients with **analgesic nephropathy**, sickle cell disease, or diabetes, none of which are indicated here.
- It often leads to **gross hematuria** and passage of tissue fragments, and can be associated with severe pain, but the clinical picture does not fit this diagnosis.
*Interstitial renal inflammation*
- Acute interstitial nephritis is often caused by **drug reactions** or infections and is characterized by a significant inflammatory infiltrate in the renal interstitium.
- While it can cause flank pain and hematuria, it more commonly presents with **fever, rash, and eosinophiluria**, and less often with prominent proteinuria like glomerulonephritis.
Kidney transplant pathology US Medical PG Question 7: A 60-year-old African American woman presents to her ophthalmologist with blurry vision. She reports a 2-month history of decreased vision primarily affecting her right eye. Her past medical history is notable for type 1 diabetes and hypertension. She takes insulin and enalapril. She has a 40-pack-year smoking history and drinks a glass of wine at dinner each night. Her family history is notable for glaucoma in her mother and severe diabetes complicated by nephropathy and retinopathy in her father. Her temperature is 99°F (37.2°C), blood pressure is 134/82 mmHg, pulse is 88/min, and respirations are 18/min. On exam, she is well-appearing and in no acute distress. The physician asks the patient to look forward and shines a penlight first in one eye, then the other, alternating quickly to observe the pupillary response to the light. When the light is shined in the right eye, both pupils partially constrict. When the light is shined in the left eye, both pupils constrict further. When the light is moved back to the right eye, both eyes dilate slightly to a partially constricted state. Where is the most likely site of this patient’s lesion?
- A. Lateral geniculate nucleus
- B. Lens
- C. Oculomotor nerve
- D. Ciliary ganglion
- E. Optic nerve (Correct Answer)
Kidney transplant pathology Explanation: ***Optic nerve***
- The alternating pupillary response, where shining light in the affected right eye causes less constriction than in the left eye, even though both pupils constrict, points to a **Relative Afferent Pupillary Defect (RAPD)**, also known as a **Marcus Gunn pupil**.
- An RAPD indicates a lesion in the **afferent visual pathway** anterior to the optic chiasm, most commonly the optic nerve, as it reduces the input signal from the affected eye to the brainstem.
*Lateral geniculate nucleus*
- A lesion in the **lateral geniculate nucleus (LGN)** would cause a visual field defect, but typically would not present with an RAPD because the pupillary light reflex pathway largely bypasses the LGN.
- The afferent pupillary fibers synapse in the **pretectal nucleus** before reaching the Edinger-Westphal nucleus, not the LGN.
*Lens*
- Problems with the **lens**, such as cataracts, cause blurry vision due to light scattering but do not affect the afferent pupillary pathway or cause an RAPD.
- The lens focuses light onto the retina; it is not involved in transmitting signals for the pupillary light reflex.
*Oculomotor nerve*
- A lesion in the **oculomotor nerve (CN III)** would affect the efferent pupillary pathway, leading to a **dilated pupil** in the affected eye, often with impaired extraocular movements, which is not described.
- The oculomotor nerve carries parasympathetic fibers responsible for pupillary constriction.
*Ciliary ganglion*
- A lesion in the **ciliary ganglion** would also affect the efferent pupillary pathway, causing a **dilated pupil** and sluggish or absent light reflex on the affected side (tonic pupil).
- This is a post-ganglionic parasympathetic lesion, which would present differently from the observed RAPD.
Kidney transplant pathology US Medical PG Question 8: A 4-month-old boy is brought to the physician for a well-child examination. He was born at 36 weeks' gestation. The mother has had no prenatal care. His 6-year-old sister has a history of osteosarcoma. He is exclusively breast fed. He is at the 60th percentile for height and weight. Vital signs are within normal limits. Examination shows inward deviation of the right eye. Indirect ophthalmoscopy shows a white reflex in the right eye and a red reflex in the left eye. Which of the following is the most appropriate next step in management?
- A. Screen for galactosemia
- B. Fundus examination (Correct Answer)
- C. Visual training exercises
- D. CT scan of the eye
- E. Serum rubella titers
Kidney transplant pathology Explanation: **Fundus examination**
- The presence of a **white reflex (leukocoria)** in the right eye is a critical finding that suggests serious ocular pathology, such as **retinoblastoma**, congenital cataract, or retinopathy of prematurity.
- A prompt **fundus examination** by an ophthalmologist is essential to identify the underlying cause and initiate appropriate treatment to preserve vision and potentially life, especially given the family history of osteosarcoma (which can be associated with retinoblastoma).
*Screen for galactosemia*
- Galactosemia can cause **cataracts**, leading to leukocoria; however, it's typically associated with other symptoms like **vomiting**, poor feeding, and **hepatomegaly**, which are not reported here.
- While screening might be considered, the immediate and most critical step is to investigate the white reflex directly.
*Visual training exercises*
- **Visual training exercises** are typically used for amblyopia or strabismus, a deviation of the eye (which is present here).
- However, they would only be considered *after* ruling out serious underlying causes of leukocoria, as the white reflex indicates a more urgent issue.
*CT scan of the eye*
- A **CT scan of the eye** could be used to evaluate for **intraocular tumors** like retinoblastoma or calcifications.
- However, a **fundus examination** is typically the initial diagnostic step to visualize the retina and determine the nature of the white reflex, guiding subsequent imaging if needed.
*Serum rubella titers*
- **Congenital rubella syndrome** can cause cataracts (leukocoria) and other ocular abnormalities.
- However, there are no other signs suggestive of congenital rubella infection (e.g., microcephaly, congenital heart defects, hearing loss), and testing for it is not the most immediate or highest priority given the acute finding of leukocoria.
Kidney transplant pathology US Medical PG Question 9: A 13-year-old boy is brought to the physician because of swelling around his eyes for the past 2 days. His mother also notes that his urine became gradually darker during this time. Three weeks ago, he was treated for bacterial tonsillitis. His temperature is 37.6°C (99.7°F), pulse is 79/min, and blood pressure is 158/87 mm Hg. Examination shows periorbital swelling. Laboratory studies show:
Serum
Urea nitrogen 9 mg/dL
Creatinine 1.7 mg/dL
Urine
Protein 2+
RBC 12/hpf
RBC casts numerous
A renal biopsy would most likely show which of the following findings?
- A. Effacement of podocyte foot processes on electron microscopy
- B. Granular deposits of IgG, IgM, and C3 on immunofluorescence (Correct Answer)
- C. Splitting and alternating thickening and thinning of the glomerular basement membrane on light microscopy
- D. Mesangial IgA deposits on immunofluorescence
- E. "Spike-and-dome" appearance of subepithelial deposits on electron microscopy
Kidney transplant pathology Explanation: ***Granular deposits of IgG, IgM, and C3 on immunofluorescence***
- This finding is characteristic of **post-streptococcal glomerulonephritis (PSGN)**, supported by the history of recent tonsillitis, periorbital swelling, dark urine, hypertension, and features of nephritic syndrome (RBC casts, proteinuria).
- The granular deposition pattern reflects the immune complex-mediated nature of PSGN, where **antigen-antibody complexes** deposit in the glomeruli.
*Effacement of podocyte foot processes on electron microscopy*
- This is the hallmark finding in **minimal change disease**, which typically presents with abrupt onset of nephrotic syndrome (severe proteinuria, hypoalbuminemia, edema) without hematuria or hypertension.
- The patient's presentation with **dark urine** (hematuria), hypertension, and RBC casts is inconsistent with minimal change disease.
*Splitting and alternating thickening and thinning of the glomerular basement membrane on light microscopy*
- This describes the characteristic changes seen in **Alport syndrome**, an inherited disorder affecting collagen IV.
- Alport syndrome presents with **hematuria**, progressive renal failure, and often includes hearing loss and ocular abnormalities, which are not mentioned in this acute presentation.
*Mesangial IgA deposits on immunofluorescence*
- This is the diagnostic feature of **IgA nephropathy (Berger's disease)**.
- IgA nephropathy often presents with **recurrent macroscopic hematuria** occurring concurrent with or shortly after an upper respiratory infection, rather than 2-3 weeks later like PSGN.
*"Spike-and-dome" appearance of subepithelial deposits on electron microscopy*
- This appearance is characteristic of **membranous nephropathy**, which is a common cause of **nephrotic syndrome** in adults.
- Membranous nephropathy typically presents with significant proteinuria and edema, and it is less common in children with acute nephritic symptoms like those described.
Kidney transplant pathology US Medical PG Question 10: A 12-year-old boy comes to the physician for the evaluation of intermittent blood-tinged urine for several months. Four months ago, he had an episode of fever and sore throat that resolved without treatment after 5 days. During the past 2 years, he has also had recurrent episodes of swelling of his face and feet. 5 years ago, he was diagnosed with mild bilateral sensorineural hearing loss. His brother died of a progressive kidney disease at the age of 23. The patient appears pale. His temperature is 37°C (98.6°F), pulse is 70/min, and blood pressure is 145/85 mm Hg. Slit lamp examination shows a conical protrusion of both lenses. Laboratory studies show a hemoglobin concentration of 11 g/dL, urea nitrogen concentration of 40 mg/dL, and creatinine concentration of 2.4 mg/dL. Urinalysis shows:
Blood 2+
Protein 1+
RBC 5–7/hpf
RBC casts rare
Which of the following is the most likely underlying cause of this patient's symptoms?
- A. IgA deposits
- B. WT1 gene mutation
- C. Defective type IV collagen (Correct Answer)
- D. Autosomal-recessive kidney disease
- E. Type II hypersensitivity reaction
Kidney transplant pathology Explanation: ***Defective type IV collagen***
- This patient presents with a classic triad of symptoms: **progressive kidney disease** (elevated creatinine, blood-tinged urine, family history), **sensorineural hearing loss**, and **ocular abnormalities** (lenticonus on slit lamp exam). These findings are highly suggestive of **Alport syndrome**, which is caused by a defect in **type IV collagen**.
- The family history of a brother dying of progressive kidney disease at a young age further supports a genetic cause, and the intermittent blood-tinged urine after an upper respiratory infection can be a feature of Alport syndrome, often misinterpreted as IgA nephropathy early in its course.
*IgA deposits*
- **IgA nephropathy** can present with recurrent episodes of gross hematuria, often following an upper respiratory infection, similar to the initial presentation of this patient's blood-tinged urine.
- However, IgA nephropathy typically does not involve **sensorineural hearing loss** or **ocular abnormalities** like lenticonus.
*WT1 gene mutation*
- A **WT1 gene mutation** is associated with **Denys-Drash syndrome** and **Frasier syndrome**, which involve nephropathy and, in some cases, gonadal abnormalities or ambiguous genitalia.
- While these can cause kidney disease, they do not typically present with the characteristic ocular findings (lenticonus) or sensorineural hearing loss seen in this patient.
*Autosomal-recessive kidney disease*
- While Alport syndrome can have autosomal recessive inheritance (10-15% of cases), this option is too broad and does not specify the underlying **molecular defect** (type IV collagen).
- The family history pattern here (affected brother, male proband) is more consistent with **X-linked Alport syndrome** (85% of cases), and this non-specific option does not pinpoint the actual pathogenic mechanism that links all the patient's symptoms.
*Type II hypersensitivity reaction*
- A **type II hypersensitivity reaction** involves antibody-mediated cellular destruction or dysfunction, such as in Goodpasture syndrome, where antibodies attack the glomerular basement membrane.
- This mechanism does not explain the long-standing, progressive nature of kidney disease combined with sensorineural hearing loss and ocular defects. Instead, these are characteristic of an underlying structural protein defect.
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