This was earlier described as acute-on-chronic-renal failure. As mentioned it was due to many different causes. Besides searching for and treating reversible causes of this clinical situation one should treat and see. However, If there is an acute  deterioration of renal function of unknown origin with large kidneys, a renal biopsy may be indicated. I remember such a case of an elderly lady with a rapidly progressive glomerulonephritis with could be successfully treated with more specific therapy.    

Acute Kidney Injury ( AKI ) on CKD can lead to rapid onset of ESRD . The common causes of AKI are sepsis , volume depletion  , nephrotoxic drugs & contrast agents . AKI is considered a reversible , but life threatening disease .  In CKD , it can cause irreversible renal failure . CKD is a risk factor for AKI . CKD causes a gradual reduction of GFR , but onset of AKI can lead to rapid onset of ESRD . It is essential to prevent AKI in patients with CKD & if it occurs it should be diagnosed & treated early to prevent SORO - ESRD . The common causes of CKD are DM & HT & AKI occurs in an ICU setting .

 SORO-ESRD should be considered a special clinical entity , as rapid progression of CKD to ESRD has enormous implications for management , because of high cost of maintenance dialysis & renal transplant . More patients with CKD are reaching ESRD much earlier than anticipated , due to AKI .

Chronic kidney disease (CKD) is when there is permanent damage to your kidneys.  Your kidneys may still work well enough for you to live, even if they have some damage.

If your kidneys keep getting worse, CKD can lead to kidney failure (ESRD).  This is when the kidneys do not work well enough for you to live.  If this happens, you will need dialysis or a kidney transplant to live.

This situation can occur after any superimposed  insult in advanced CKD eg severe infection, general anesthesia, radiologic contrast media, surgery, deshydration but seems more frequent in diabetic nephropathies (and amyloidosis). After a search for a curable cause (for instance urologic obstruction) and a careful follow up of patients waiting for partial or total recovery the only way of management is often to begin dialysis.

Thanks all for your instructive responses.

I just wonder if beyond classical known causes of insult, there is a genetic basis of  SORO-CKD. For instance some variants of APOL1 gene were found to be associated with more rapid GFR decline in some types of CKD.

I do not know if SORS-CKD exists as advertized. It is described as a rapid, non-linear deterioration of eGFR. What is non-linear for sure is eGFR. The low end of eGFR is rather unrelated to GFR for a number of reasons, not the least of which is that eGFR from creatinine overestimates GFR. That is, even creatinine clearance from exogenous creatinine overestimates GFR more severely as tubular excretion becomes predominant for lower GFR values. Moreover, the eGFR estimating formulas are not precise for any endogenous creatinine level, and especially not in severe renal insufficiency. Yet more problems are introduced by the unphysical units used. Normalization by estimated body surface area is just sad, it is not physical. So, does SORS-CDK exist? I am sure that rapid deterioration occurs. But before one can prove that this has anything to do with non-linearity, one needs to use a linear yardstick. As far as I can tell at first glance, mind you, I do not see this as an established entity. Oh, and please do correct me if I am wrong.

I agree clinicians and researchers should speak the same language; it is all about helping people. Let's start somewhere. How about, body surface area does not cause urine to form? The spurious variable is height in the BSA formulas, using weight to a power without height gives better correlations, and adding in (measured) interstitial volume to a power improves the correlation markedly (Nucl Med Commun. 2006;27(12):963-70). At the moment, constant infusion of inulin is the only commonly used method of determining GFR that is not highly suspect. It has problems in end stage renal disease as the infusion time to equilibrium becomes intractably long. GFR (inulin) does not scale to the same power of body weight as Cr-CL does (Adolph, Science 1949). One does not have to scale GFR at all if one is using the patient as his own control in time, gross GFR is enough. Intensive management could include dumping the spurious correlations to avoid potential harm. If I were doing the management, I would want to know what the GFR really is. I have published methods of finding GFR in difficult situations, but, they are not widely read. I suspect it is difficult to decide what therapy does what when given the non-linearity of eGFR and that there may be a benefit of examining suspected SORO-ESRD using linear GFR measurement systems to figure out what the effects of our therapies are. Worse, neither GFR nor percentage change of GFR  are normally distributed, although percentage change is more "linear".

I agree: this situation can occur after any superimposed insult in advanced CKD eg sepsis, acute descompensated heart failure, general anesthesia, contrast-induced nephropathy, surgery, dehydration, drug nephrotoxicity. (As a pediatric intensivist I can confirm this frequently).

And I agree too: SORO-ESRD is not a specific clinical entity.

What is important is prevent these modifiable factors whenever possible. Once we can do nothing about the non-modifiable factors for CKD progression: periods of rapid growth (such as puberty), race (racial susceptibility may be present in African Americans compared to Caucasian) and certain genetics polimorphisms of the ACE gene.