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Prednisone and creatinine levels.Corticosteroids (methylprednisolone, prednisone) |
- Prednisone - Uses, side effects, dosage | National Kidney Foundation
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Prednisone and creatinine levels -
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A corticosteroid course of 12 months was given. Patients were observed for a mean follow up of 84 months.
Despite similar lesion severity at renal biopsy, renal function stabilized only in these two ones. In conclusion, these preliminary observations suggest a possible efficacy of corticosteroids in slowing down the progression of renal disease and in postponing the need of dialysis in IgAN patients with stage IV CKD and severe chronic histological lesions. According to the Italian Register of Dialysis and Transplantation, in about patients started dialysis because of a glomerulonephritis [ 1 ].
The presence of diffuse chronic lesions at renal biopsy, which is a common finding in these patients, stands against active treatment. However, the histological picture cannot be considered the only factor driving therapeutic choices. This, together with the fear of adverse events and the lack of large randomized clinical trial also in IgAN patients with normal or only mildly reduced renal function till the end of nineties, led to some therapeutic nihilism.
However, these agents neither can prevent patients reaching rapidly ESRD nor can act on immunological mechanisms, which may remain active also in the more advanced stages of the nephropathy.
A 6-month course of corticosteroids halted the progression of renal disease for six years, indicating that sometimes corticosteroids could modify the course of IgAN also in the so-called late-referral patients [ 6 ]. None of these patients was previously aware of having advanced CKD, and the hypothesis of the need of renal replacement therapy in the near future terrified them.
So, they asked us to carry out a treatment to avoid or to postpone that need. The patients underwent clinical and biochemical controls every three months to evaluate the clinical course and to recognize possible side effects of corticosteroids.
These patients were followed for a mean of 84 months range 72— A year-old man IE with a previous history of hypertension treated with candesartan was admitted in our unit in May for CKD stage IV serum creatinine of 3.
Immunofluorescence supported the diagnosis of chronic IgA nephropathy. Corticosteroid were given for one year. Proteinuria rapidly decreased, reaching values of 0. Because of high proteinuria, six months later a new 6-month course of steroids was performed obtaining a new decrease of proteinuria 0. Renal function remained stable during the whole follow up of months Figure 1.
No important side effects due to corticosteroids were observed. He was receiving fosinopril because of hypertension lasting 10 years. Baseline clinical characteristics are reported in Table 1. According to immunofluorescence findings, a diagnosis of chronic IgA nephropathy was made. The patient received a month steroid therapy without significant side effects. Serum creatinine remained stable till month 60, then rapidly increased.
Dialysis was started after 72 months of follow up Figure 1. Hypertension had been known sincebut enalapril was started only a few weeks before admission. Vessels were not evaluable. A diagnosis of chronic IgA nephropathy was made. A corticosteroid course of 12 months was given without side effects. Serum creatinine remained stable 3. On immunofluorescence basis, a diagnosis of chronic IgA nephropathy was made. Corticosteroids were given for one year.
Proteinuria decreased to 0. Serum creatinine remained stable for 42 months, then increased up to 4. The second corticosteroid course obtained a temporarily halt of progression for the next six months Figure 1.
The overall follow up was of 78 months. Important side effects due to corticosteroids were not observed. In advanced chronic nephropathies, progression seems to be mainly driven by nonimmunological processes. However, histological indexes of activity can also be detected, especially in rapidly progressive patients. Immunosuppressive therapies may potentially reverse proliferative and essudative lesions as much as possible and prevent a further development of glomerular and tubular sclerosis.
Indeed, although the pathophysiologic processes ultimately leading to fibrosis are complex, proliferative and essudative lesions could amplify cytokine and growth factor cascades enhancing interstitial infiltration and fibroblast activity.
Following treatment, renal function and proteinuria behaved differently in the single patients of these case reports. These data are in line with the concept that the lower proteinuria is during follow up, the better the outcome is [ 910 ]. However, for the first time they suggest that this prognostic factor is of value also in patients with advanced IgAN and that the rate of proteinuria decrease following treatment may be of importance as well.
To confirm these preliminary observations, we evaluated the relationship between proteinuria behaviour following treatment and CKD progression in 38 IgAN patients with stage III-IV CKD having adequate follow up more than 48 monthswho were enrolled in a multicentre, clinical trial comparing steroids plus azathioprine to steroids alone and followed up for at least 48 months [ 7 ]. Despite the lack of a control group and the small number of this case series, these data suggest that steroid therapy may slow down progression of CKD also in patients with advanced IgAN.
Our preliminary results are in line with two studies comparing the efficacy of ACE-I alone versus ACE-I plus corticosteroids demonstrating that the addition of steroids resulted in a better renal outcome and in a more potent antiproteinuric effect [ 1213 ].
However, differing from this case series, the enrolled patients had a normal or a slightly reduced renal function. The majority were retrospective and enrolled patients with more preserved renal function than our case series, allowing the use of more aggressive regimens including azathioprine, cyclophosphamide, or mycophenolate mofetil MMF.
Goumenos et al. However, the same authors were not able to confirm their positive findings in another retrospective study of 74 patients observed for a longer follow up period [ 15 ]. Mitsuiki et al. Treatment-related side effects were observed in only two patients. The treated patients experienced significantly better renal survival and a greater reduction in proteinuria levels than those in the control group.
More recently, Roccatello et al. Following treatment, serum creatinine and proteinuria significantly dropped at 6 months compared with baseline values and remained lower during a mean follow up of 51 months range 24— However, none of them compared cytoxic agents plus steroids to steroids alone.
According to the findings of our recent trial [ 7 ], in CKD patients stage III-IV a small likelihood of reducing the risk of CKD progression with steroids plus azathioprine compared to steroids alone should be well balanced with an increased risk of side effect with the adding of azathioprine to treatment.
Finally, would the pathological features of our patients been able to predict their renal outcome and treatment response? The answer is no. Traditional classifications of IgAN do not offer enough information to decide which patient deserves treatment [ 19 — 24 ].
In addition, all the four renal biopsies showing advanced damage with a prevalence of diffuse chronic lesions were against a possible usefulness of corticosteroids. In conclusion, these preliminary observations suggest a possible efficacy of corticosteroids in slowing down the progression of the renal disease and in postponing the need of dialysis in IgAN patients with stage IV CKD and severe chronic histological lesions.
D'Amico, A. Ragni, E. Gandini, and G. Wastl, T. Risler et al. Komatsu, S. Fujimoto, Y. Sato et al. Hou, X. Zhang, G. Zhang et al. Pozzi, L. Del Vecchio, and F. Pozzi, S. Andrulli, A. Pani et al. In press. Pozzi, P. Bolasco, G. Fogazzi et al. Reich, S. Troyanov, J.
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The GFR is the main, but not the single, determinant of the plasma creatinine levels. Several drugs, such as cimetidine, trimethoprim, corticosteroids. To clarify the rise in plasma creatinine concentration previously observed during prednisone treatment, we studied. Prednisone is part of a group of drugs called corticosteroids (often called "steroids"). Other steroid drugs include prednisolone. We conclude that GFR rises during 2 weeks of high-dose prednisone administration, a rise that is not reflected by a decrease in plasma creatine concentration. The other S symbols indicate a doubling of admission creatinine levels, and are significantly different between prednisone (two) and control (11). Medicine and Health. A very serious allergic reaction to prednisone is rare. In advanced chronic nephropathies, progression seems to be mainly driven by nonimmunological processes.Cholesterol embolism is a disease that is attracting growing attention [ 1 ]. It typically complicates intravascular catheterization and anticoagulant and thrombolytic therapy, during which atheromatous materials are dislodged from major vascular walls and occlude small arteries of multiple organs.
Many organs may be affected, and typical features include a purpuric rash, livedo reticularis, myalgia, and acute renal failure. Once cholesterol emboli have occurred, therapy is of limited value. Intensive supportive treatments including haemodialysis are usually needed. Information on the use of corticosteroids in this condition is limited and its effects are controversial.
The patient had a long over 10 years history of hypertension, diabetes mellitus, renal dysfunction as well as anterior myocardial infarction in He developed intermittent claudication in in the right calf, and recent similar symptoms in the left calf.
Angiography of the lower limbs demonstrated multiple occlusive lesions. A saccular abdominal aortic aneurysm was also found following CT. Coronary angiography performed on October 19 showed severe lesions in the anterior descending artery. A percutaneous transluminal coronary angioplasty PTCA with stenting was performed on October 28 prior to the surgery. The patient's serum creatinine was slightly elevated 2.
It increased to 3. The patient was transferred to the renal division on November Upon transfer, he was unwell with nausea, right lumbar pain and mild fever. The bilateral dorsalis pedis pulse was good. No skin lesions such as livedo reticularis were found.
The chest was clear according to percussion and auscultation. Palpation of the abdomen revealed a tenderness at the right hypochondrium. The haemoglobin was There was a hypocomplimentaemia of CH50 C3 at Chest radiography was unremarkable. A renal ultrasonographic study showed bilateral atrophic kidneys right 8. A diagnosis of an acute episode of chronic renal failure due to cholesterol embolism was made for the following reasons: i an increase of serum creatinine occurred after more than a week following coronary angiography and PTCA, ii both peripheral blood eosinophilia and iii hypocomplementaemia were observed.
As no skin lesions, such as livedo reticularis were present, skin biopsies were not feasible and histopathologic proof of cholesterol emboli was not obtained. Serum creatinine levels, which reached a peak of Creatinine was 3. The clinical symptoms of mild fever, malaise, abdominal discomfort, and eosinophilia subsided.
Serum creatinine increased to 4. No further increase in serum creatinine level was observed. The temporal course of serum creatinine in a patient with cholesterol embolism treated with prednisolone. Cholesterol embolism is an important and often underdiagnosed cause of renal insufficiency [ 1 ].
Cholesterol crystals originate in large vessels such as the abdominal aorta and then lodge in small arteries, such as the arcuate, interlobular and terminal arterioles of the kidneys. The subsequent intravascular inflammatory reaction causes tissue ischaemia and ultimately leads to renal failure.
Cholesterol embolism also involves the skin, muscles, abdominal organs and central nervous system, resulting in significant morbidity and mortality. Performing a skin, muscle, or renal biopsy often allows an accurate diagnosis. Predisposing factors include vascular surgery, arteriography, angioplasty, anticoagulation and thrombolytic therapy.
Unlike in contrast nephropathy, renal failure due to cholesterol embolism develops about a week after the vascular procedure and persists or progresses over weeks and months. The patient presented here already had moderate renal impairment upon admission.
A rapid deterioration of renal function occurred following coronary angiography, PTCA, and abdominal aortic aneurysm resection and graft surgery. Due to a lack of skin lesions and to renal atrophy, no biopsy was feasible. The present patient had eosinophilia and a high sedimentation rate.
He also had hypocomplimentaemia, which is often associated with cholesterol embolism. Based on the presence of predisposing factors, the clinical manipulations, eosinophilia, high sedimentation rate and hypocomplementaemia, a final diagnosis of an acute episode of chronic renal failure due to cholesterol embolism was made.
The prognosis of cholesterol embolism is usually ominous, and information on specific treatments is limited. Measures that are usually recommended include i discontinuation of anticoagulant treatment, ii avoidance of further aortic catheterization, iii control of hypertension, iv haemodialysis, and v nutritional support.
Corticosteroid therapy has been utilized to reduce the inflammatory response with limited or no success. A recent report from Belenfant et al. They administered 0. It was not specified in the report to what extent corticosteroid treatment improved renal function nor whether it contributed to the overall improvement of patients' prognoses.
To our knowledge, the cholesterol embolism case presented here is the first showing rapid improvement in renal function and avoidance of haemodialysis following a small dose of oral corticosteroid prednisolone 0. Despite this being a single case experiment and the lack of histopathologic diagnosis, our experience suggests that corticosteroid treatment may be warranted in cholesterol embolism.
A study with a larger number of patients may give more definitive directions for the use of corticosteroids as a treatment for cholesterol embolism. Atheroembolic renal disease. Semin Nephrol ; 16 : — Redefining the incidence of clinically detectable atheroembolism. Am J Med ; : — Incidence of atheroembolic renal failure after coronary angiography. Angiology ; 48 : — Cholesterol embolism: experience with 22 histologically proven cases. Surgery ; 82 : — Supportive treatment improves survival in multivisceral cholesterol embolism.
Am J Kid Dis ; 33 : — Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account. Sign In. Advanced Search. Search Menu. Article Navigation.
Close mobile search navigation Article Navigation. Volume Article Contents Case. Journal Article. Small dose oral corticosteroid treatment rapidly improved renal function in a patient with an acute aggravation of chronic renal failure due to cholesterol embolism. Hajime Nakahama , Hajime Nakahama. Oxford Academic. Google Scholar. Katsuhiko Sakaguchi. Select Format Select format. Permissions Icon Permissions. Sir, Cholesterol embolism is a disease that is attracting growing attention [ 1 ].
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