Suffering from ankylosing spondylitis for decades, this "pain reliever" was always available at home, and the kidney broke down in the end...

Only for medical professionals to read for reference.
When ankylosing spondylitis merges with renal damage, how to "break" it? Case review Patient Zhang, a 55-year-old male, was admitted to the hospital with "found elevated blood creatinine with nausea and edema of both lower extremities for 1 week"
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1 week before admission, patients with a history of present illness have no obvious causes of nausea, vomiting, dizziness, mild swelling of the lower limbs, no headache, no fear of cold, fever, chest tightness, no shortness of breath, no oliguria, foamy urine, no rash, or photosensitivity , No oral ulcers, joint swelling and pain, no abdominal pain and diarrhea and other discomforts, go to the local hospital, check creatinine: 288μmol/L, glomerular filtration rate (GFR): 18.
43ml/min, B-type natriuretic peptide (BNP): 35000pg/ml, CT of the upper abdomen showed: low-density focus of right kidney, bilateral pleural effusion, pericardial effusion, enlarged heart shadow
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After the sacroiliac joint CT film treatment, the above symptoms did not improve significantly (the specific diagnosis and treatment is unknown), and the edema of both lower limbs gradually increased, accompanied by oliguria, foamy urine, cough, yellow sputum, and asthma, so he went to a third-class hospital in Fuzhou Measure blood pressure 200/145mmHg, check "urea nitrogen: 20.
92mmol/L, creatinine: 311μmol/L"
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Diagnosis: Renal insufficiency, cardiac insufficiency, lung infection, hypertension, treated with "hypertension, cardiotonic diuresis, coronary expansion, anti-infection" and other treatments, the symptoms improved significantly
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I am going to the nephrology department of our hospital today, and I plan to be admitted to the hospital for "research on the cause of renal insufficiency"
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The patient has been mentally exhausted recently, can sleep soundly, and has not seen any significant changes in weight recently
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The patient complained of repeated low back pain for more than 30 years, which was persistent, increased after early rest, relieved after exercise, accompanied by low back stiffness, gradually unable to squat, restricted waist movement, and increased after fatigue in recent years
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For the past 30 years, I took 5-6 tablets of "Quietong Tablets" by myself every day, the pain can be relieved a little, and there is no diagnosis and treatment
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Admission examination T: 36.
3℃, P: 63 beats/min, R: 20 beats/min, BP: 137/85mmHg, no tenderness in the sternum, normal thoracic motion, 10cm distance between occipital walls, restricted spine flexion and extension , Schober test positive, lumbosacral tenderness (+), left "4" test (+), straight leg elevation test, left (-) enhancement (+), right (-) enhancement (-), double The lower limbs were slightly edema, muscle strength and muscle tension were normal, and pathological signs were not elicited
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The initial diagnosis on admission 1.
Chronic renal insufficiency; 2.
Cardiac insufficiency; 3.
Pulmonary infection; 4.
Hypertension grade 3 (very high risk)
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Auxiliary examination of blood cell analysis: WBC: 7.
6×109/L, HGB: 132g/L↓, HCT: 0.
381l/L, PLT: 149.
0×109/L
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Hypersensitive CRP: 43.
60mg/L; ESR: 86mm/h; Procalcitonin: 0.
424ng/ml, BNP: 19850pg/ml
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Four items of coagulation+D-D+FDP+AT3: FIB: 5.
58g/l↑, D-2 polymer: 0.
54mg/L↑, the rest is normal
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Biochemical set: albumin: 31.
8g/L↓, BUN: 22.
28mmol/L, CREA: 304.
1μmol/L, uric acid: 573.
6μmol/L, GFR: 18.
9
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ANA (titer) + ds-DNA + ENA: negative HLA-B27: 94.
0%↑ premature renal damage: urine creatinine: 4866.
2μmol/L, microalbumin: 236mg/L, microprotein/urine creatinine: 48.
50mg/mmol , 24h urine protein: 1.
010g/24h urine routine: urine protein: 1+, the rest is normal
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Urine protein electrophoresis: a variety of protein components can be seen, suggesting mixed proteinuria.
This week’s protein electrophoresis: there are no different monoclonal bands in each lane.
Urine protein is negative.
Abnormal immunoglobulinemia.
Serum light chain: serum Kappa light.
Chain: 1.
87g/L (1.
38~3.
75), serum Lambada: 1.
68g/L (0.
93~2.
42), serum Kappa light chain/Lambada light chain: 1.
1131Ratio↓ Serum immunoglobulin: IgA: 1.
43g/L; IgG : 8.
84g/L; IgM: 0.
43g/L.
Serum protein electrophoresis: M protein bands are found.
It is recommended to combine the analysis of serum immunofixation electrophoresis results: M: 0.
54% ECG: 1.
Sinus rhythm; 2.
Left ventricular overload , Suggesting left ventricular hypertrophy; 3.
ST~T change, abnormal U wave
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CT of the sacroiliac joint and both adrenal glands: 1.
CT of the bilateral adrenal glands showed no obvious abnormalities
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2.
Scan and scan bilateral pleural effusion, scan and pericardial effusion
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3.
Bilateral sacroiliitis symptomatic lesions (considering the possibility of ankylosing spondylitis), please combine with clinical laboratory examinations
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4.
Scan multiple cystic translucent shadows on both sides of the acetabulum, considering degenerative changes
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Lung CT: inflammation of the lower lobes of both lungs, it is recommended to review after treatment; a small amount of effusion in the pericardium and both sides
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Fundus examination: hypertensive retinopathy in both eyes; optic disc edema in the right eye
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Analysis and further examination of this patient with repeated low back pain for more than 30 years, and HLA-B27 was positive.
After consultation with our department, this patient met the diagnostic criteria for ankylosing spondylitis (AS) revised in 1984: (1) Low back pain lasted for 3 months Above; (2) The direction of anteroposterior and lateral flexion of the lumbar spine is restricted; (3) CT of the sacroiliac joints suggests: bilateral sacroiliac arthritis is grade 3 to 4, so AS can be diagnosed, and thalidomide is recommended to suppress immunity, rheumatism Department outpatient follow-up
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In addition, the patient was admitted to the hospital for serum protein electrophoresis: M protein bands were found; serum immunofixation electrophoresis: abnormal monoclonal bands were found in IgG and λ lanes, and the type of monoclonal immunoglobulin was IgG λ, and the hematology consultation considered multiple myeloma The results of complete bone marrow aspiration + pathology and immunophenotyping of multiple myeloma are as follows: bone marrow routine: bone marrow slice: the proportion of plasma cells is slightly higher, accounting for about 4%, and they are all mature plasma cells
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Opinion: Three-line hyperplasia, increased proportion of plasma cells, please combine clinical, flow cytometry and immunofixation electrophoresis
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Bone marrow pathology: HE and PAS staining showed low bone marrow hyperplasia (30%-40%), reduced granule red ratio, and granular red cells can be seen at various stages, mainly in the middle and juvenile and below stages, and erythroid and various stages of cells can be seen , Mainly in the middle and late young red blood cells, the number of megakaryocytes is roughly normal; a small number of lymphocytes and plasma cells are scattered
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Multiple myeloma immunophenotyping: flow cytometry results suggest that about 0.
4% of abnormal plasma cells can be seen in the submitted specimens, and the intracellular immunoglobulin Kappa/Lambda light chain clone is not obvious
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 Currently diagnosed: 1.
Chronic kidney disease (CKD) stage 4; 2.
Ankylosing spondylitis; 3.
Plasma cell disease; 4.
Hypertension grade 3 (very high risk) binocular hypertensive retinopathy; 5.
Heart failure; 6.
Double pneumonia
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After admission, the patient's symptoms improved after treatments such as antihypertensive, cardiotonic, diuretic, anti-infection, supplementation of essential amino acids, and thalidomide suppression of immunity
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AS and its complications may cause kidney damage.
AS is a chronic progressive inflammatory spondyloarthritis, usually onset with sacroiliitis, which can cause spine slubularity and even disability
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The onset of some ASs is insidious and the symptoms are not severe, causing the patients to fail to seek medical treatment in time, delay the diagnosis, and delay the treatment
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AS can be accompanied by extra-articular manifestations, such as uveitis and iritis, kidney damage, aortic valve insufficiency, and upper pulmonary fibrosis and cystic degeneration
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It has been reported in the literature that the incidence of renal damage in AS patients is 5% to 13%, and the consequences are serious, which is one of the main causes of end-stage death in AS
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AS patients currently considered kidney damage common types are the following: renal amyloidosis, IgA nephropathy, non-steroidal anti-inflammatory analgesics (NSAIDs) such as kidney damage correlation
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Renal amyloidosis has been reported in foreign literature.
Secondary renal amyloidosis accounts for about 1.
1% of AS patients.
Amyloidosis can be divided into different types of fibrin deposited: AL protein amyloidosis, AA protein amyloidosis and other thyroid glands.
Carrier protein amyloidosis, but there are few clinical reports, and the current mechanism is still unclear
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IgA nephropathy is the most common pathological type of renal damage secondary to AS
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Relevant studies have shown that AS and IgA nephropathy have the same immune characteristics, and the levels of serum IgA and related immune complexes in these patients usually increase
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IgA nephropathy is the most common glomerulonephritis, which can be primary or secondary
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IgA nephropathy is characterized by the deposition of IgA in the basement membrane of the kidney, which leads to repeated hematuria, which can also be manifested as asymptomatic proteinuria or hematuria under microscope
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For the treatment of AS combined with IgA nephropathy, there is nothing special, and ACE inhibitors have been proven to have achieved good results
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NSAIDs-related renal damage AS is a chronic disease.
Patients have a history of long-term short-term use of NSAIDs due to low back pain.
These drugs have a certain impact on renal function
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In the normal population, 1% to 5% of people have adverse renal reactions due to the side effects of drugs (including NSAIDs)
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The mechanism of the influence of NSAIDs on renal function is currently considered to be mainly as follows: ①By inhibiting vasodilator prostaglandins, it changes the renal blood flow and glomerular filtration rate, causing kidney damage; ②Inducing the reduction of prostaglandin synthesis, leading to intermittent The formation of qualitative nephritis; ③Acute and chronic renal papillary necrosis
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There are few cases of membranous glomerulonephritis with membranous nephropathy.
It is difficult to distinguish whether the two diseases coexist because of etiology or simply coexist
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The most difficult clinical problem in the tragedy caused by drug abuse is that AS is a disease that requires long-term treatment.
When kidney damage occurs in patients with AS, it is difficult to distinguish whether AS combined with kidney damage is caused by the progression of the disease itself or Because of the adverse reactions of the drugs, and sometimes the drugs taken by the patients during the course of the disease are not only the NSAIDs drugs
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In this article, the patient had repeated low back pain for more than 30 years, and took 5-6 tablets of "Tong Pain Tablets" by himself every day to relieve pain
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Pain relief tablets mainly contain aminopyrine, phenacetin, phenmabitone and other ingredients
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Among them, aminopyrine and phenacetin are antipyretic and analgesic drugs (belonging to NSAIDs) and are the main drugs; phenmabitone is also known as lumina, which has a sedative and hypnotic effect to improve pain and irritation, but long-term use is easy to cause Addiction, and tolerability, a few enhancement doses are needed to obtain the original curative effect; long-term use of phenacetin is prone to addiction
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The harm of misuse of Pain Relief Tablets is far more than addictive, and there are other serious side effects
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For example, aminopyrine has an adverse effect on the hematopoietic system, and can cause agranulocytosis in allergic patients, which is fatal
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Even if it interacts with food under gastric acid conditions, it can also form carcinogenic nitrosamines, especially nitrosamines.
Long-term use of phenacetin-containing preparations can cause renal papillary necrosis, interstitial nephritis, etc.
, and may even Induces renal pelvic cancer and bladder cancer
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This patient found elevated blood creatinine with nausea and edema of both lower limbs for 1 week
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After admission, two and a half pairs of hepatitis B, ANA and other autoimmune indicators are all negative, and the patient has no history of diabetes, so hepatitis B-related kidney damage, connective tissue disease kidney damage and diabetic nephropathy can be ruled out
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The patient found that the blood pressure was elevated for 1 week.
The blood pressure was not monitored normally.
The electrocardiogram showed that the left ventricle was overloaded, and the fundus examination revealed hypertensive retinal changes.
The possibility of hypertensive kidney disease cannot be ruled out
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The patient was admitted to the hospital for immunofixation electrophoresis and showed M protein bands, suggesting the possibility of multiple myeloma.
The results of bone biopsy did not meet the diagnostic criteria for multiple myeloma, suggesting plasma cell disease
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The patient was advised to undergo nephrectomy to further clarify the cause of renal damage, but he refused
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The author analyzes that the renal damage in this patient with AS has many factors: combined with the patient’s medical history, it is currently considered that the long-term use of "pain-removing tablets" is the most likely to cause renal damage, and the possibility of renal damage caused by the primary disease of AS is not ruled out.
In addition, renal damage caused by plasma cell diseases and hypertension may also be one of the reasons
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The treatment instructed patients to immediately stop using "pain-removing tablets", avoid using drugs that may cause kidney damage, conduct regular diagnosis and treatment, closely monitor urine routine and renal function, erythrocyte sedimentation rate, CRP, 24-hour urine protein quantification and other indicators, and review bone marrow aspiration and quantification if necessary Improve the kidney biopsy to confirm the diagnosis
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