Overlooked Symptoms of Acute Kidney Failure

The kidneys have a central role in the human organism. Kidney dysfunctions affect blood pressure regulation, electrolyte, water, and acid-base balance as well as blood formation and bone metabolism. Nephrology, therefore, covers a wide range of diseases, and doctors of other disciplines are repeatedly facing nephrological problems.

Some cases of acute renal failure are described below, which can be used by both general practitioners and clinicians, and require a differential diagnosis.

A 33-year-old patient presented with back pain in our emergency room. In the past week, he had suffered from headache and body aches, which is why he had taken a total of 2,800 mg ibuprofen (seven 400 mg tablets) for five days. The use of performance-enhancing substances, drugs, or dietary supplements was denied. Pre-existing allergic bronchial asthma was known, but regular medication was not given. Clinical evidence of infection or systemic disease did not exist. On targeted inquiries, he stated that he had cleared his cellar about three weeks ago.

Renal Diagnostics

The examination findings revealed an elevated body temperature of 38.2 ° C as well as a knocking pain over the left kidney stock. Further vital signs and organ status were unremarkable.

Laboratory diagnostics yielded creatinine of 2.2 mg / dl (0.7 to 1.2) and urea 54 mg / dl (19 to 44) in serum (i.p.); Electrolytes, acid-base balance and blood count were unremarkable. Due to the acute renal failure, sonography of the kidneys was performed. Both kidneys were enlarged (> 12 cm, normal value 10 to 12 cm) with hypoechoic parenchyma and dedifferentiated marrow-cortical border in the sense of acute renal damage. A urinary blockage could be excluded. In further laboratory diagnostics, immune serology (ANA, ANCA, anti-GBM) was inconspicuous. Hantavirus serology was also negative. In the urine examination, there was a protein excretion of 0.6 g / g creatinine (<0.1). The urine sediment showed isolated leucocytes, no erythrocytes and was therefore not indicative of a glomerular disease in which a so-called "active sediment" with dysmorphic erythrocytes (acanthocytes) would be expected.

Due to the later increasing creatinine i. S. to the max. 3.12 mg/dl was the indication for renal biopsy. Histopathology showed an interstitial inflammatory cell infiltrate with eosinophilia and edema, consistent with drug-toxic interstitial nephritis, in this case after taking non-steroidal anti-inflammatory drugs (NSAIDs), as well as a severe tubular necrosis

Diagnosis of Acute Kidney Failure

Acute renal failure in drug-induced acute interstitial nephritis (AIN).

Treatment Courses

After the medication was discontinued, the creatinine dropped after a few days so that no immunosuppressive therapy became necessary. The diuresis was preserved at all times; with the increased recovery of the renal function set a polyuric phase, the fluid deficit was compensated with oral fluid substitution. At the time of discharge, creatinine i. S. at 1.7 mg/dl, in further outpatient controls, a creatinine was recorded.

The back pain initially leading to the admission can be explained by the swelling of the kidneys. We discussed with the patient the need in the future to consistently avoid taking ibuprofen and other NSAIDs, including in the form of ointments.

The AIN usually corresponds to an "allergic" hypersensitivity reaction in the kidneys and is most commonly caused by the intake of drugs, but can also be triggered by infections or systemic diseases. Theoretically, any medicine can cause an issue. The onset of the disease is between three days and several weeks after ingestion of the triggering agent. The development of a drug-induced is not dose-dependent and may reoccur again at any time when the same or a related drug is taken yet. Therefore, useful patient information is essential to prevent re-exposure.

Pathophysiologically, a variety of factors are involved. In addition to neurohumoral dysregulation, as in our case, increased central venous pressure with the reduced venous return from the kidneys plays a role. It has consistently been shown that increased central venous pressure correlates more with the occurrence of renal failure than, for example, reduced cardiac output due to forward failure of the left ventricle. Correspondingly, with an increased central venous pressure of about 21 mmHg, the GFR is reduced by about 26 percent.

The simultaneous presence makes the diagnosis of cardiac and renal insufficiency. As far as possible, other forms of renal insufficiency should be excluded, although here too mixed pictures occur. Findings such as active urinary sediment or significant proteinuria greater than 1 g / g creatinine suggest primary kidney damage.

Specific therapy of CRS would be an improvement of the cardiac function or a reduction of the pulmonary-arterial pressure. Since this is often not possible, the consequent but gentle volume compensation is in the foreground. Often, diuretics must be given intravenously, as enteral absorption is limited due to decompensation. With the obtained negative balance improves, as in the case described, the venous return from the kidneys, and there is a consequent increase in renal function. In the case of failure of conservative therapy for volume reduction, extracorporeal ultrafiltration, for example, by dialysis, is the next therapy step. In chronic dialysis due to a CRS, the continuous procedure of peritoneal dialysis is of particular importance.

References

https://www.niddk.nih.gov/health-information/kidney-disease/kidney-failure

https://www.hopkinsmedicine.org/gim/research/content/ckd.html

https://stemcellthailand.org/therapies/renal-failure-kidney-disease/

https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(15)60944-8/fulltext